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Biomedical subjects

C Rampulla

Publications and source records attributed to C Rampulla.

At least 37 records · Page 2Linked to original sources

Breathing pattern, ventilatory drive and respiratory muscle strength in patients with chronic heart failure.

The purpose of this study was to evaluate whether chronic heart failure (CHF) may induce changes in breathing pattern and ventilatory neural drive. We studied 45 male inpatients with CHF, (25 patients in NYHA class II, 20 in class III) and 22 sex-matched post myocardial infarction patients without left ventricular dysfunction who served as controls. CHF patients underwent right heart catheterization and assessment of cardiac output by thermodilution technique. Patients and controls underwent evaluation of left ventricular ejection fraction by 2D echocardiography, spirometry, diffusion capacity, blood gases, breathing pattern, mouth occlusion pressure and respiratory muscle strength determination. Results of CHF patients were compared to controls and evaluated for differences according to the degree in severity of functional impairment. CHF patients showed a slight reduction in lung volumes and in diffusion capacity. In CHF neural drive, as assessed by mouth occlusion pressure (P0.1), was significantly increased in comparison to controls (P0.1 = 1.86 (0.7) and 1.4 (0.6) cmH2O in CHF and controls respectively). Analysis of breathing pattern showed only a slight yet significant increase in respiratory frequency while respiratory muscle strength, as assessed by measurement of maximal inspiratory and expiratory pressures (MIP and MEP respectively) was slightly reduced (MIP = 79(27) and 104(28); MEP = 111(32) and 142(33) cmH2O respectively). Observed changes were more relevant in patients with advanced NYHA functional classes whereas no relationship among indices of cardiac and respiratory function was found. We conclude that chronic heart failure induces changes in neural ventilatory drive and respiratory muscle strength related to the severity of the disease.

Cardiac Output↗

Survival and prediction of successful ventilator weaning in COPD patients requiring mechanical ventilation for more than 21 days.

We studied survival and failure or success of weaning from mechanical ventilation (MV) in 42 consecutive chronic obstructive pulmonary disease (COPD) patients requiring prolonged MV (more than 21 days) after an episode of acute respiratory failure requiring admission to our Intermediate Intensive Care Unit (IICU). Parameters including arterial blood gases, pulmonary function tests, respiratory muscle force, neuromuscular drive, and nutritional status were recorded during a phase of clinical stability, in order to identify the features related to survival and weaning. All the patients were submitted to a comprehensive rehabilitation programme. Successful weaning from MV was defined as complete respiratory autonomy for at least 48 h. Twenty three patients were successfully weaned from MV after an average period of 44 days (Group A), requiring no further MV during their stay in hospital, whilst the remaining 19 patients were not able to be disconnected from the ventilator (Group B). The discriminant analysis showed that weaning from MV was significantly associated with arterial carbon dioxide tension (PaCO2), neuromuscular drive (P0.1), maximal inspiratory pressure (MIP), arterial oxygen tension (PaO2), the ratio of respiratory frequency to tidal volume (f/VT) and the serum protein level. Other pulmonary function tests (forced expiratory volume in one second (FEV1), FEV1/forced vital capacity (FVC), anthropometric data, nutritional status, number of pulmonary exacerbations during MV and evidence of cor pulmonale, were similar in the two groups. The discriminant equation considering PaCO2 and MIP could separate the two groups with an accuracy of 84%. The overall survival at 2 yrs was 40%; in Group B it was significantly lower than in Group A (22 vs 68%). Most of the deaths occurred within the first 120 days after intubation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Hypophosphatemia and phosphorus depletion in respiratory and peripheral muscles of patients with respiratory failure due to COPD.

In 22 patients (19 men, 3 women; mean [+/- SD] age, 63 +/- 6 years) with chronic obstructive pulmonary disease (COPD), phosphorus content was measured by spectrophotometric methods on muscle fragments of both peripheral (quadriceps femoris needle biopsy in 22 patients) and respiratory muscles (external intercostal muscle surgical biopsy in 14 patients). Thirty age- and sex-matched subjects were used as controls (19 for quadriceps femoris muscle biopsy and 11 for intercostal muscle biopsy). Serum phosphorus levels, as well as the main determinants of overall phosphorus metabolism (dietary intake of phosphorus and renal phosphate handling), were also obtained in all patients and control subjects. Muscle phosphorus content of both respiratory and peripheral muscles was significantly reduced in the COPD patient group, no matter what reference index was used (fat-free dry muscle weight or muscle fragment DNA content); muscle phosphorus depletion was present in about 50 percent of patients with COPD. In the same patient group, a significant relationship between muscle and serum phosphorus levels was demonstrable in the case of peripheral muscles only. No relationship was found between phosphorus content of both types of skeletal muscles and dietary phosphorus intake levels or with nutritional status, even though patients with COPD had significantly reduced anthropometric, biochemical, and immunologic indices as compared with controls. Renal phosphorus handling indices of the COPD patient group were compatible with a condition of inadequacy of the renal compensatory mechanism to hypophosphatemia and phosphorus depletion (low percent tubular reabsorption of phosphorus, low renal threshold concentration values). Our study suggests that phosphorus depletion occurs frequently in COPD, but in this clinical condition serum phosphorus levels are not representative of cellular phosphorus levels. Phosphorus depletion, which is equally severe in respiratory and peripheral muscles, could depend, at least in part, on malnutrition and a condition of renal phosphorus wasting possibly linked to some drugs commonly used in patients with COPD (xanthine derivatives, diuretics, etc).

Aged↗

Pidotimod in the treatment of patients affected by bacterial exacerbations of chronic bronchitis.

A multicentre double-blind placebo-controlled study was conducted in order to assess the effects of pidotimod ((R)-3-[(S)-(5-oxo-2-pyrrolidinyl) carbonyl]-thiazolidine-4-carboxylic acid, PGT/1A, CAS 121808-62-6), a new synthetic biological response modifier, on the clinical picture of bacterial exacerbations of chronic bronchitis. Seven centres of respiratory diseases participated in the trial. A total of 137 patients, 103 males and 34 females (mean age: 65.0 years) were admitted to the study. The trial was subdivided into 3 phases. During the first 8-day phase (D0-D8), 68 patients received 800 mg pidotimod orally (one sachet) twice daily and an antibiotic treatment (amoxycillin plus clavulanic acid: 1 g twice daily), while 69 patients received placebo (one sachet) and antibiotic according to the same dosage schedule. In the second 7-day phase (D8-D15), while the double-blind therapy proceeded, the antibiotic treatment was stopped. The third phase (D15-D45) consisted of a 30-day follow-up period. Five clinical observations, at D0, D4, D8, D15 and D45, were scheduled. The Skin test, to evaluate immunocompetence, was carried out at D0, D15 and D45. The faster improvement of symptomatology (dyspnoea, cough, sputum, hyperpyrexia) in the patients in the pidotimod group compared with the placebo group was reflected in recovery time: mean 8.9 days in the pidotimod group versus 10.7 days in the placebo group (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Haemodynamic effects of pressure support and PEEP ventilation by nasal route in patients with stable chronic obstructive pulmonary disease.

BACKGROUND: Intermittent positive pressure ventilation applied through a nasal mask has been shown to be useful in the treatment of chronic respiratory insufficiency. Pressure support ventilation is an assisted mode of ventilation which is being increasingly used. Invasive ventilation with intermittent positive pressure, with or without positive end expiratory pressure (PEEP), has been found to affect venous return and cardiac output. This study evaluated the acute haemodynamic support ventilation by nasal mask, with and without the application of PEEP, in patients with severe stable chronic obstructive pulmonary disease and hypercapnia. METHODS: Nine patients with severe stable chronic obstructive pulmonary disease performed sessions lasting 10 minutes each of pressure support ventilation by nasal mask while undergoing right heart catheterisation for clinical evaluation. In random order, four sessions of nasal pressure support ventilation were applied consisting of: (1) peak inspiratory pressure (PIP) 10 cm H2O, PEEP 0 cm H2O; (2) PIP 10 cm H2O, PEEP 5 cm H2O; (3) PIP 20 cm H2O, PEEP 0 cm H2O; (4) PIP 20 cm H2O, PEEP 5 cm H2O. RESULTS: Significant increases in arterial oxygen tension (Pao2) and saturation (Sao2) and significant reductions in arterial carbon dioxide tension (PaCO2) and changes in pH were observed with a PIP of 20 cm H2O. Statistical analysis showed that the addition of 5 cm H2O PEEP did not further improve arterial blood gas tensions. Comparison of baseline values with measurements performed after 10 minutes of each session of ventilation showed that all modes of ventilation except PIP 10 cm H2O without PEEP induced a small but significant increase in pulmonary capillary wedge pressure. In comparison with baseline values, a significant decrease in cardiac output and oxygen delivery was induced only by the addition of PEEP to both levels of PIP. CONCLUSIONS: In patients with severe stable chronic obstructive pulmonary disease and hypercapnia, pressure support ventilation with the addition of PEEP delivered by nasal mask may have short term acute haemodynamic effects in reducing oxygen delivery in spite of adequate levels of SaO2.

Aged↗

Recruitment of some respiratory muscles during three maximal inspiratory manoeuvres.

BACKGROUND: A study was undertaken to determine the level of recruitment of the muscles used in the generation of respiratory muscle force, and to ascertain whether maximal diaphragmatic force and maximal inspiratory muscle force need to be measured by separate tests. The level of activity of three inspiratory muscles and one expiratory muscle during three maximal respiratory manoeuvres was studied: (1) maximal inspiration against a closed airway (Muller manoeuvre or maximal inspiratory pressure (MIP)); (2) maximal inspired manoeuvre followed by a maximal expiratory effort (combined manoeuvre); and (3) maximal inspiratory sniff through the nose (sniff manoeuvre). METHODS: All the manoeuvres were performed from functional residual capacity. The gastric (PGA) and oesophageal (POES) pressures and their difference, transdiaphragmatic pressure (PDI), and the integrated EMG activity of the diaphragm (EDI), the sternomastoid (ESTR), the intercostal parasternals (ERIC), and the rectus abdominis muscles (ERA) were recorded. RESULTS: Mean (SD) PDI values for the Muller, combined, and sniff manoeuvres were: 127.6 (19.4), 162.7 (22.2), and 136.6 (24.8) cm H2O, respectively. The pattern of rib cage muscle recruitment (POES/PDI) was similar for the Muller and sniff manoeuvres (88% and 80% respectively), and was 58% in the combined manoeuvre, confirming data previously reported in the literature. Peak EDI amplitude was greater during the sniff manoeuvre in all subjects (100%) than during the combined (88.1%) and Muller (61.1%) manoeuvres. ESTR and EIC were more active in the Muller and the sniff manoeuvres. The contribution of the expiratory muscle (ERA) to the three manoeuvres was 100% in the combined, 26.1% for the sniff, and 11.5% for the Muller manoeuvre. CONCLUSIONS: Each of these three manoeuvres results in different mechanisms of inspiratory and expiratory muscle activation and the intrathoracic and intra-abdominal pressures generated are a reflection of the interaction between the various muscle groups. The Muller and sniff manoeuvres reflect mainly the force of the inspiratory muscles and the combined manoeuvre that of the diaphragm.

Adult↗

Expiratory airflow limitation and hyperinflation during methacholine-induced bronchoconstriction.

To investigate the role of airflow limitation on the increase of end-expiratory lung volume (EELV) during bronchoconstriction, nine stable asthmatic subjects and seven healthy subjects were challenged with inhaled methacholine (MCh). Changes in airway caliber were assessed by using forced expiratory volume in 1 s, partial forced expiratory flow at 50% of control forced vital capacity, and specific airway conductance. To detect airflow limitation, tidal flow-volume curves were superimposed on partial forced flow-volume curves at absolute lung volume. The electromyogram of the diaphragm was recorded by surface electrodes in four asthmatic and four healthy subjects, and the electrical diaphragmatic activity (DIA) during expiration was expressed as a percentage of the duration of expiratory time. In 10 subjects (9 asthmatic and 1 healthy) the partial forced expiratory flow recorded after some MCh dose impinged on tidal expiratory flow recorded before MCh. When this occurred it was associated with an increase in EELV by 0.54 +/- 0.07 (SE) liter (P < 0.001), which was larger than that occurring when lower MCh doses (0.11 +/- 0.04 liter, P < 0.05) were used, and with a moderate increase in DIA of 15 +/- 2.5% (P < 0.01). Six healthy subjects did not increase EELV after MCh despite a significant degree of bronchoconstriction; in these subjects tidal expiratory flow never impinged on forced expiratory flow, and DIA never increased. These results suggest that hyperinflation during MCh-induced bronchoconstriction is triggered by dynamic compression of the airways and is associated with moderate increase of DIA during expiration.

Adolescent↗

Effect of pressure and timing of contraction on human rib cage muscle fatigue.

Breathing against inspiratory loads can be accomplished with different degrees of coupling between the diaphragm and the other muscles attached to the rib cage (RCM). Thus, the electromyographic signs of fatigue develop separately in each muscle group. While breathing with diaphragm emphasis, the occurrence of diaphragmatic fatigue was found to be related to the tension-time index TTdi (= Pdi/Pdimax x Ti/Ttot). Above the critical range of 0.15 to 0.18, the endurance of the diaphragm is less than 1 h and it is inversely related to the TTdi value. However, in most loaded breathing conditions, the spontaneous pattern of breathing is characterized by predominant activation of RCM. The tension-time conditions at which fatigue develops during breathing with RCM emphasis are not known. We assessed the critical tension-time value in four normal subjects breathing with RCM emphasis against inspiratory threshold loads. RCM predominance was achieved by developing negative abdominal pressure swings during inspiration, and it was characterized by the tension-time index TTrc (Ppl/Pplmax x Tl/Ttot), where Ppl is pleural pressure developed under this condition. Above a critical TTrc value of 0.30, endurance time was inversely related to TTrc, and it resulted from failure of the RCM rather than of the diaphragm. We conclude that the critical threshold, as assessed by TTrc, is higher for breathing patterns with RCM emphasis than previously described by TTdi for diaphragm emphasis. However, when predominantly recruited, as in breathing patterns commonly adopted in loaded conditions, the RCM fatigue earlier than the diaphragm.

Adult↗

Effect of nasal pressure support ventilation and external PEEP on diaphragmatic activity in patients with severe stable COPD.

Nasal pressure support ventilation (NPSV) has been shown to be useful in the treatment of acute and chronic pulmonary failure. However, little is known about respiratory muscle activity during NPSV in stable patients with COPD. The aim of this study was to test the effect of two levels (10 and 20 cm H2O) of NPSV on diaphragmatic activity, in a group of seven stable, severe COPD patients (FEV1 20 percent +/- 7 of pred, FEV1/FVC 35 percent) with hypercapnic respiratory insufficiency. Since these patients had an intrinsic PEEP (PEEPi) of 2.6 +/- 1.3 cm H2O, we also investigated the effect of adding 5 cm H2O external PEEP (PEEPe) during NPSV. Blood gases, ventilatory pattern by inductive plethysmography, integrated electromyogram of the diaphragm (Edi), transdiaphragmatic pressure (Pdi), and the diaphragmatic pressure time product (PTPdi) were recorded during randomized 15-min runs of both levels of NPSV with and without the addition of PEEPe. Minute ventilation did not change with the application of NPSV, but a significant decrease in breathing frequency with a parallel increase in tidal volume was observed, so that blood gas determinations improved at the higher levels of support. A marked statistically significant reduction in diaphragmatic activity, as assessed by a decrease in Pdi swings, PTPdi, and Edi, was detected at the levels of 10 and 20 cm H2O; a further significant decrease in these values was observed when PEEPe was added. PEEPi decreased significantly only with the application of PEEPe, resulting in a small increase in end-expiratory lung volume. We conclude that NPSV improves diaphragmatic function in patients with severe stable COPD; this effect may be enhanced by the applications of external PEEP.

Aged↗

Effect of long-term therapy with oral steroids on respiratory muscle function and ventilatory drive.

It has been shown that chronic oral steroid therapy (ST) does not induce respiratory muscle dysfunction in normal and asthmatic subjects. As corticosteroids are sometimes chronically used in the treatment of the patients with chronic obstructive pulmonary disease (COPD), the aim of our study was to verify whether ST could cause respiratory muscle impairment and, since ST also affects the central nervous system, whether ST could influence the ventilatory pattern. We retrospectively studied 12 COPD patients (group A), on long-term therapy (for at least 4 consecutive months, range 4-18 months) with an oral steroid, deflazacort, 15 mg.d-1. The subjects were strictly matched, with regard to age, sex, height, weight, forced expiratory volume in one second (FEV1), residual volume (RV), arterial oxygen tension (PaCO2), arterial carbon dioxide tension (PaCO2) and pH, with 12 COPD patients (Group B) who had never taken oral steroids. To assess respiratory muscle strength, we measured maximal inspiratory (MIP) and expiratory (MEP) pressures, while mouth occlusion pressure (P0.1) was employed to assess neuromuscular drive; ventilatory pattern and airway impedence were also evaluated. Effectiveness of ST was confirmed by the plasmatic levels of endogenous cortisol. No significant differences were observed between the two groups with regard to MIP (A 72.2 +/- 9.7 vs B: 70 +/- 7.2 cmH2O) and MEP (A 91.6 +/- 10.5 vs B 94.4 +/- 7.6 cmH2O) whilst P0.1 was significantly higher in group A (2.6 +/- 0.3 cmH2O) than in group B (1.8 +/- 0.1 cmH2O). No significant differences were found among all the ventilatory parameters, but the impedence was significantly higher in group A.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Evidence of acute diaphragmatic fatigue in a "natural" condition. The diaphragm during labor.

Acute diaphragmatic fatigue has been experimentally shown to occur in normal healthy subjects and in patients with chronic obstructive pulmonary disease by asking them to modify their pattern of breathing or to breathe against high inspiratory resistances. During the expulsive period of labor women are asked periodically to make strong expulsive efforts and to sustain them isometrically for many seconds; this is likely to produce "natural" diaphragmatic fatigue. To investigate whether this was the case, six women were studied in the delivery room from the moment of the rupture of the amnion until delivery of the infant occurred. The development of diaphragmatic fatigue was assessed both by measuring the static maximal inspiratory pressure (MIP) and by analyzing the electromyographic power spectrum of the diaphragm (H/L ratio). The majority of contractions were concentrated in the expulsive period of labor. MIP, recorded in the supine position, significantly decreased from 103.2 +/- 17.2 cm H2O (at the beginning of the expulsive period) to 73.8 +/- 10.1 cm H2O (after the delivery). The H/L ratio fell progressively during the expulsive period; after the delivery, it was 59.2 +/- 15.7% of the value recorded at the beginning of the expulsive period. This study demonstrates that (1) the diaphragm is active in the expulsive efforts during labor and (2) the tension developed and the time each contraction is maintained may lead to the development of diaphragmatic fatigue. Therefore, we provide evidence of acute diaphragmatic fatigue in a natural condition.

Acute Disease↗

Effect of a beta 2-agonist (broxaterol) on respiratory muscle strength and endurance in patients with COPD with irreversible airway obstruction.

The effect of broxaterol, a new beta 2-agonist, on respiratory muscle endurance and strength was studied in a double-blind, placebo-controlled, randomized crossover clinical trial in 16 patients with chronic obstructive pulmonary disease (COPD) with irreversible airway obstruction (FEV1 = 57.1 percent of predicted). One patient withdrew from the study because of acute respiratory exacerbation. Inspiratory muscle strength was assessed by maximal inspiratory pressure (MIP) and endurance time was determined as the length of time a subject could breathe against inspiratory resistance (target mouth pressure = 70 percent of MIP, Ti/Ttot = 0.4). Broxaterol (B) or placebo (P) was given orally for seven days at the dose of 0.5 mg three times a day with a washout period of 72 h between study treatments. Measurements were performed before administration of B or P and 2 h (six patients) or 8 h (nine patients) after the end of each treatment. No significant changes in FEV1 or FRC were observed after B or P suggesting that diaphragmatic length was maintained constant with each treatment. The MIP did not significantly change, while endurance time increased after B in the patients tested at 2 h (from 234.8 +/- 48.1 s to 284.0 +/- 48.0 s, p less than 0.05) and at 8 h (from 187.2 +/- 31.1 s to 258.2 +/- 40.4 s, p less than 0.005). No changes were observed after P. Minute ventilation, airway occlusion pressure (P0.1), integrated electromyographic activities of the diaphragm (Edi), and intercostal parasternals (Eic) (normalized to the value obtained during MIP) showed no change during the endurance run with different treatments. We conclude that in a group of COPD patients with irreversible airway obstruction, B significantly improves respiratory muscle endurance, and that this does not arise as a result of an effect on neuromuscular drive or pulmonary mechanics, but may be mediated by peripheral factors.

Adrenergic beta-Agonists↗