AIDS-associated Cryptococcosis causing adult respiratory distress syndrome.
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Biomedical subjects
Publications and source records attributed to T Similowski.
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Assessing diaphragmatic contractility is a common goal in various situations. This assessment is mainly based on static or dynamic maximal voluntary maneuvers and twitch transdiaphragmatic pressures (Pdi) obtained by stimulation of the phrenic nerves (PS). PS eliminates the central components of diaphragmatic activation, but the available techniques of PS remain subject to some limitations. Transcutaneous PS is painful, and needle PS is potentially dangerous. Time-varying magnetic fields can stimulate nervous structures without pain and without adverse effects. In six subjects, we have studied cervical magnetic stimulation (CMS) as a method of PS. We have compared the stimulated Pdi (Pdistim) with the maximal Pdi obtained during static combined expulsive-Mueller maneuver (Pdimax) and with the Pdi generated during a sniff test (Pdisniff). CMS produced twitch Pdi averaging 33.4 +/- 9.7 cmH2O. Pdistim/Pdimax and Pdistim/Pdisniff were 24 +/- 6 and 41 +/- 14%, respectively. These values are comparable to those obtained in other studies with transcutaneous PS. They were highly reproducible in all the subjects. Electromyographic data provided evidence of bilateral maximal stimulation. CMS is a nonspecific method and may stimulate various nervous structures. However, diaphragmatic contraction was elicited by stimulation of the phrenic trunk, since the phrenicodiaphragmatic latencies (less than 7 ms) were in the range of values reported with direct stimulation of the trunk. Cocontraction of neck muscles, including the sternomastoid, was present, but its influence in the CMS-induced Pdi seems minimal. We conclude that magnetic stimulation is an easy, well-tolerated, reproducible safe, and valuable method to assess phrenic conduction and diaphragmatic twitch response.
Pulmonary and chest wall mechanics were studied in six anesthetized paralyzed dogs, by use of the technique of rapid airway occlusion during constant flow inflation. Analysis of the pressure changes after flow interruption allowed us to partition the overall resistance of the lung (Rl) and chest wall (Rw) and total respiratory system (Rrs) into two components, one (Rinit) reflecting in the lung airway resistance (Raw), the other (delta R) reflecting primarily the viscoelastic properties of the pulmonary and chest wall tissues. The effects of varying inspiratory flow and inflation volume were interpreted in terms of frequency dependence of resistance, by using a spring-and-dashpot model previously proposed and substantiated by Bates et al. (Proc. 9th Annu. Conf. IEEE Med. Biol. Soc., 1987, vol. 3, p. 1802-1803). We observed that 1) Raw and Rw,init were nearly equal and small relative to Rl and Rw (both were unaffected by flow); 2) Rrs,init decreased slightly with increasing volume; 3) both delta Rl and delta Rw decreased with increasing flow and increased with increasing lung volume. These changes were manifestations of frequency dependence of delta R, as it is predicted by the model; 4) Rrs, Rl, and Rw followed the same trends as delta R. These results corroborate data previously reported in the literature with the use of different techniques to measure airways and pulmonary tissue resistances and confirm that the use of Rl to assess bronchial reactivity is problematic. The interrupter techniques provides a convenient way to obtain Raw values, as well as analogs of lung and chest wall tissue resistances in intact dogs.
Hypercapnia is common in chronic respiratory failure (IRCO), and may be further increased in a significant way by oxygen therapy, used for severe hypoxaemia in acute exacerbations. The determinants of PaCO2 are metabolic (hence importance of alkalosis) and ventilatory. In chronic airflow obstruction, CO2 production and ventilation are normal; thus the factor responsible for hypercapnia is essentially the fraction of total ventilation lost in the anatomical and alveolar (VD/VT ratio) dead space, whose effect on PaCO2 is all the more marked on account of the high starting point. From the time of administering pure oxygen hypercapnia is only weakly linked to changes in total ventilation (which, after a few minutes returns to its initial level) and only slightly to the correction of hypoxaemia and desaturation (Haldane effect). On the other hand, the ventilation-perfusion ratios are altered, as evidenced by increased VD/VT ratios. The exact mechanisms are ill understood, but one could consider the worsening venous admixture effect by the reduction of hypoxic vasoconstriction and micro-atelectasis in the poorly ventilated zones, as well as the rise in the anatomical dead space (broncho-dilatation) and alveolar dead space (redistribution of ventilation to poorly perfused zones). In comparison with standard ideas, the genesis of hypercapnia from oxygen therapy depends more on an AIR/BLOOD mis-match, than on the suppression of the hypoxic ventilatory stimulus.
The stimulation of the phrenic nerves in the neck is one of the techniques for the examination of diaphragmatic contractility. Current methods are restricted by their painful (transcutaneous stimulation) or even potentially dangerous nature (needle stimulation). We have tested both the feasibility and the validity of using magnetic stimulation (SMC) to stimulate the phrenic nerves. This method is painless and devoid of any side effects. Three healthy subjects have been studied using an EMG and transdiaphragmatic pressure measurements (Pdi.) Pdi values obtained by SMC (36.5 +/- 13.5 cm H2O) and their relation to maximal Pdi (22.6 +/- 7%) and to the Pdi at the time of maximal sniff-Pdi sniff (34.7 +/- 8%) were comparable to those values obtained using other methods and were reproducible. The preliminary results show that SMC is a technique for the study of the phrenic nerve and diaphragm which has the advantage of simplicity in use, is repeatable and is completely innocuous.
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