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Biomedical subjects

E L De Vito

Publications and source records attributed to E L De Vito.

17 recordsLinked to original sources

[Functional respiratory evaluation in patients with high traumatic spinal injury].

The restrictive defect was quantified (Forced vital capacity, FVC) and their postural dependence and the respiratory muscle weakness (Maximal inspiratory and expiratory pressures, MIP and MEP) in 29 patients (12 to 46 years) with spinal injury from cervical (C) 4 to thoracic (T) 7 (30 days to 48 months post injury period). The FVC in C (seated) was 2200 +/- 560 ml (47.2%), and in T was 2940 +/- 750 ml (66.6%), p < 0.008. The postural dependence of the FVC was higher in C with an increase of 25% and only of 10% in the T (p < 0.03). This postural dependence was a function of the FVC according to the regression equation: FVC % (supine) = 24.73+ 0.7341* FVC % seated (r 0.8771, p < 0.001). The MIP in C was 61.59 (53.82%) +/- 17.26 cm H2O and in T was 87.25 (77.85%) +/- 24.27 cmH2O (p < 0.05). The MEP in C was 48.53 (24.97%) +/- 18.09 cm H2O, and in T was 58.75 (30.74%) +/- 27.67 cmH2O (p NS). No correlation was found between FVC and maximal statics respiratory pressures. In conclusion, the C showed more significant restrictive defect and a great postural dependence of the FVC. In both, the expiratory muscle weakness was more severe than the inspiratory group. Inspiratory muscle weakness was higher in C.

Adolescent↗

Effects of spontaneous and hypercapnic hyperventilation on inspiratory effort sensation in normal subjects.

In order to elucidate if the inspiratory effort sensation (IES) associated with carbon dioxide (CO2) is independent of the concomitant increase in the ventilation, we studied 23 normal resting volunteers (mean age 34 +/- 11 yr) during CO2 rebreathing. Our main goal was to compare the IES at the same ventilation level under hypercapnic and isocapnic conditions. The protocol included: (1) basal measurements (BASAL); (2) hypercapnic ventilation (HV); (3) screen copy of ventilatory pattern during hypercapnia (COPY); (4) screen copy at basal end-tidal (partial) carbon dioxide pressure (PETCO2) (ISO); and (5) recovery (REC). During HV, PETCO2 increased to 54.8 +/- 0.78 mm Hg (p < 0.001) and ventilation (VE) from 12.0 +/- 0.50 to 28.1 +/- 1.19 L/min (p < 0.001). Borg value increased from 0.11 +/- 0.06 to 3.4 +/- 0.23 (p < 0.001). These values were not different during HV and COPY. During ISO, PETCO2 was 40.2 +/- 0. 59 mm Hg (not significant [NS] from BASAL), while VE remained unchanged: 29.9 +/- 1.29 L/min (NS from HV and COPY). Interestingly, the Borg value during the ISO decreased to 1.86 +/- 0.28 (p < 0.001 compared with HV and COPY). The increased IES induced by hypercapnic ventilation was reduced at the same ventilation level during isocapnic conditions. We suggest that CO2 generates an IES independent of the concomitant increase in ventilation.

Adult↗

Bilateral diaphragmatic paralysis after mediastinal radiotherapy.

A 35-year-old man presented bilateral phrenic paralysis 7 months after radio-therapy for treatment of Hodgkin's lymphoma. Diaphragmatic dysfunction appeared after complete lymphoma remission and 4 months after chemotherapy discontinuation. There were no other potential causes. Idiopathic diaphragmatic paralysis was unlikely because it is usually unilateral. Radiation-induced neuropathy is well documented in other nerves as the brachial plexus. The timing, the applied dose and the location of the nerve within the radiation field are suggestive of radiation-induced phrenic nerve damage. Partial recovery was achieved after 4 years' follow-up.

Adult↗

[Clinical and spirometric alterations in patients with Duchenne muscular dystrophy].

In 36 patients with Duchenne muscular dystrophy we studied the growth pattern, the type and severity of the spirometric abnormalities, the evolution of the Motor Functional Class (MFC), the infectious complications and treatments. Their age ranged from 6 to 19 years and the MFC was from 1 to 9. Regarding height, up to 12 years we verified a slope of 5.69 +/- 0.58 cm/year (r 0.872 p < 0.001) and a posterior detention was observed. Of the 36 patients, 24 were below the percentile 5. The restrictive disorder prevailed. The forced vital capacity (FVC) expressed in % of the theoretical value showed a lineal fall with age, with a negative correlation (r 0.51, p < 0.01) of -3.5 +/- 0.83%/year. The deterioration of the MFC was marked starting from 6 years; with a slope of 0.84 +/- 0.14 points between 6 to 12 years (r 0.73 p x 0.001). Up to 14 years, the slope was 0.212 +/- 0.084 (r 0.49, p < 0.05). Patients older than 14 years had reached a greater CFM of 7; starting from this MFC a progressive fall of the VC was observed with a slope of -15.29 +/- 3.39% of CVF/CF (r 0.56, p < 0.001). Nine patients with respiratory infections were documented. Four were pneumonia and 3 of them required mechanical ventilation and died. Only 50% of the patients accepted rehabilitating treatment. Four patients accepted surgery of the alterations of the feet while the patients with deformation of the column underwent spinal stabilization.

Adolescent↗

[Effects of experimental ascites on diaphragm strength].

We studied the strength developed by the diaphragm during progressive ascitis induction (40 up to 280 ml/kg wt) and the changes in the radium of curvature in relation with its strength in 6 anesthetized dogs. Force generation of the diaphragm was assessed with the Pdi obtained with bilateral phrenic nerve stimulation at 60 Hz. In relation to increases in the abdominal liquid, the thoraco-pulmonary compliance decreases (p < 0.05) from 10.1 to 6.8 ml/kg/cm H2O. The radius of curvature increases 158% from the basal values; the calculated basal tension was 347 +/- 43, final 448 +/- 32 cm H2O/cm. The diaphragmatic length in percent of the basal value was 138%. The X-rays findings showed cephalic displacement, diaphragmatic flattening and stretching. The Pdi obtained should be the result of a complex interaction between the diaphragmatic geometry, the length, the degree of stretching during the contraction and preload. We can describe the changes in Pdi in 2 steps: initial increase and final decrease, associated to high Pga at the beginning and a low one later. First the Pdi increases by the Pga without significant changes in the Pes. The fact is that an increase in Pga can be related with cephalic displacement of the diaphragm with stretching and shortening of the radius of curvature and decreases in the abdominal compliance. The final decreases in the Pdi could be related with overstretching and decreases of the radius of curvature.

Analysis of Variance↗

[Central alveolar hypoventilation with cor pulmonale: successful treatment by non-invasive intermittent positive pressure ventilation].

A 62 year-old woman with a bilateral carotid body paraganglioma presented, 2 years after the removal of the right one, with signs of right-heart failure. Hypoxemia, hypercapnia, polycythemia and pulmonary hypertension with normal ventilatory capacity were found. Central alveolar hypoventilation was diagnosed on the basis of absence of ventilatory response and sensation of provoked hypercapnia, prolonged breath-holding time and correction of hypercapnia by voluntary ventilation. Progesterone (200 mg/d during 3 weeks) or naloxone did not improve either arterial blood gases (ABG) or the P 0.1/PCO2 curve. Hypoxemia and hypercapnia were not corrected during metabolic acidosis provoked by acetazolamide (250 mg/d). Nasal CPAP did not control hypoventilation periods. Mechanical ventilation was initiated with negative pressure (NPV) through a poncho. The patient presented severe discomfort with NPV and obstructive apneas were verified during it. She refused to continue NPV. Mechanical ventilation was initiated with positive intermittent pressure (IPPV) through a nasal mask. The patient had excellent tolerance to the procedure. SpO2 during IPPV was always higher than 95%. During sleep induction (under IPPV), respiration in phase with the ventilator 1: 1 was observed; instead, during consolidated sleep there was a complete dependence of the ventilator with apnea for over 2 min when IPPV was interrupted (Fig. 1). After 2 months of treatment, a relief of right ventricular failure occurred and hematocrit fell to 39%. There was an improvement of day-time ABG (Table I). The P. 0.1/PaCO2 curve 3 months after IPPV was the same as the previous one (Fig. 2). The patient has been for 18 months on home ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗

Central and peripheral diaphragmatic fatigue in loaded normal and vagotomized dogs.

Severe inspiratory elastic load terminated by respiratory arrest (RA) was studied in 24 anesthetized dogs (group 1, normal: n = 14; group 2, vagotomized: n = 10). The peripheral and central components of the decrease in diaphragmatic force generation and the events preceding RA were studied. We measured stimulated tetanic transdiaphragmatic pressure (Pdi), single twitch compound action potentials, integrated diaphragmatic electromyographic activity (iEMGdi), respiratory frequency (f), inspiratory time, inspiratory drive, overall diaphragmatic activation, and Pdi single twitch superimposed over peak Pdi. Imposed target pressure was -68.8 +/- 4.37 cmH2O for group 1 and -70.9 +/- 4.19 cmH2O for group 2, and the tension-time index of the diaphragm was the same for both groups (0.22 +/- 0.010). During load, 1) f increased in group 1 from 25.4 +/- 1.33 to 41.3 +/- 4.66 cycles/min, and tachypnea was prevented by vagotomy; 2) twitch occlusion persisted until RA and compound action potentials did not change; 3) iEMGdi and inspiratory drive increased and remained high until RA; 4) overall diaphragmatic activation increased 514 (group 1) and 260% (group 2) and then decreased to 228% of the basal value 10 s before RA in group 1 because of a fall in f; and 5) after RA, Pdi stimulated at 60 Hz fell to 39 (group 1; P < 0.0025) and 51% (group 2; NS with group 1) of the basal value. In summary, 1) peripheral fatigue developed without transmission failure; 2) diaphragmatic activation remained maximal until RA; 3) the fall in f appeared as a preterminal event only in group 1; and 4) vagus nerves are necessary for load-induced tachypnea.

Action Potentials↗

[Causes of CO2 retention in patients with chronic obstructive lung disease].

The mechanisms of chronic ventilatory failure in chronic obstructive pulmonary disease are complex. This paper analyses the diverse available information: mechanical factors and gas-exchange, fighter vs. non-fighter, the ventilatory pattern theory and the fatigue threshold theory. Finally we comment on the evidence supporting the new concept that hypercapnia may develop to avoid or prevent fatigue. Indeed, it is very likely that chronic CO2 retention in COPD may develop by mechanical disadvantages of the inspiratory muscles rather than impairment of ventilation-perfusion ratios. This opens a fascinating new research line on the neuromechanical control of breathing. When the respiratory effort is approaching the fatigue level, the respiratory muscles may elicit a negative feedback reflex, the muscle activity is depressed and hypercapnia develops. If this is so, chronic hypercapnia may be an index of imminent fatigue if increases in ventilation or work of breathing are required. Under this condition some degree of central diaphragm fatigue may help to protect the muscle from severe or limiting peripheral fatigue or even muscle injury. Finally, we comment on some therapeutic approaches such as ventilatory stimulants, training, rest and, specially, oxygen administration and the mechanisms involved in the PCO2 increases.

Humans↗

[Diaphragmatic reserve strength in obese patients].

Nine obese patients (OB) and seven normal subjects (N) were studied in order to determine diaphragmatic strength reserve, measured in terms of diaphragm Tension/Time Index (TTdi). This index was measured with the patients awake and during the obstructive apnea (OA) episodes. TTdi was 2.7 times superior in the OB (p < 0.0005) and was related with a lower Pdi Max (102 vs 202 cm H2O; p < 0.005) and with a higher Pdi (9 vs 6 cm H2O; p < 0.05). During OA the TTdi was higher than the threshold value to develop diaphragmatic fatigue (0.15-0.20) in three patients. This value was not exceeded in one patient because of striking paradoxical diaphragmatic movements. As for anthropometric data, DPI% range was higher and wider in OB (Table 1). The pCO2 in OB was 40 +/- 6 mmHg. In all patients (Table 3), severe hypoxia and hypercapnial were observed. TTdi evolution in an OA in 4 patients can be appreciated in Figure 3. It can be concluded that the diaphragmatic strength reserve is reduced in OB so that they are more susceptible to develop diaphragmatic fatigue. A fatigant respiratory pattern was also registered during the OA.

Adult↗

[Diaphragmatic strength and ventilatory control in experimental hypothermia].

In ten lightly anaesthetized dogs breathing spontaneously, we studied diaphragmatic force generation (Pdi 10, 30, 100 Hz and single twitch) and ventilatory control (P 0, 1, Vt/Ti and respiratory frequency). We found CO2 retention proportional to hypothermia (Fig. 3). The TP was not changed while VMxA and VMxD decreased (Table 1). High frequency fatigue and low frequency potentiation were found (Fig. 1, 2). These changes do not explain CO2 retention which correlated with fall in central drive (P 0, 1, Vt/Ti, Fig. 3, 4) and respiratory timing (respiratory frequency, Fig. 4).

Animals↗

[Diaphragmatic fatigue in hypovolemic shock].

A model of hemorrhagic shock (arterial mean pressure = 40 mmHg) terminated by death in all cases was developed in 21 dogs. The study was addressed to investigate the central respiratory response, development of diaphragmatic fatigue (FD) and the influence of the suppression of spontaneous rhythmic respiratory muscle activity by mechanical ventilation during shock. We measured diaphragmatic force: transdiaphragmatic pressure (Pdi), spontaneous and stimulated electrical activity of the diaphragm (integrated and rectified electromyogram: Edi) tracheal occlusion pressure (P 0, 1) cardiac output (Q) and survival, ventilatory variables were also measured. We constructed Pdi/Frequency and Pdi/Edi curves. The phrenic nerves were stimulated: 1) by bipolar electrodes at the 5th cervical roots or 2) by a bipolar electrode catheter introduced through the left jugular vein. The animals were divided in 3 groups: 1) during spontaneous breathing (light pentobarbital anesthesia and positive corneal reflex) Pdi/Frequency curves and Pdi response to single twitch were measured (n = 9); 2) evolution of Edi and Pdi/Edi curves during spontaneous breathing (n = 6); 3) Pdi/Frequency curves (n = 6) during mechanical ventilation (ARM). We found (groups 1, 2) initially compensated (increased P 0, 1 and hyperventilation: table 1) metabolic acidosis, followed by mixed acidosis after FD (fall in Pdi/Frequency: Fig. 1, and Pdi/Edi: Fig. 2, 3, table 3) and associated with falling respiratory frequency (Fr). During hyperventilation, central respiratory drive/minute: Edi.Ti.Fr (Ti = inspiratory time, sec) increased and fell later during FD, remaining however higher than basal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of aminophylline and verapamil upon diaphragmatic force generation in dogs.

The effects on the diaphragm of verapamil (VPM) and aminophylline (AMP) were studied in dogs during stimulation of phrenic nerves at the 5th cervical roots (5th-PS) or transvenously at the trunk (T-PS). Transdiaphragmatic pressure (Pdi)/frequency curves were constructed. Our findings were: 1) AMP increased Pdi at all stimulation frequencies (p less than 0.01) during 5th-PS but only at 10-30 Hz during T-PS; 2) in other dogs infusion of VPM (0.14 mg.kg-1.min-1) decreased Pdi at all frequencies (p less than 0.025) without change in diaphragmatic blood flow; 3) the effects of VPM were completely reverted by AMP; 4) after a large amount of AMP, infusion of VPM (0.21 mg.kg-1.min-1) decreased Pdi at all frequencies. Since these drugs have several mechanisms of action and do not show mutual blocking effect, different action sites are suggested.

Aminophylline↗

[Hypothermia].

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Body Temperature Regulation↗