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Biomedical subjects

A Harf

Publications and source records attributed to A Harf.

At least 181 records · Page 10Linked to original sources

[Automated monitoring of respiratory parameters in the anesthetized patient in mechanical respiration].

The constant monitoring of respiratory elastance and resistance can be of interest in patients who present a high risk of peroperative bronchospasm. The constant inspiratory flow method, proposed by Bates et al. (J Appl Physiol, 58: 1840, 1985) was chosen and automated. The inspiratory flow rate and pressure were measured respectively by a pneumotachograph linked to a differential pressure, and by a differential pressure transducer, both placed at the outlet of the inspiratory circuit. The pressure and flow signals were low-pass filtered, sampled, and then processed by an Apple II microcomputer, in order to obtain respiratory elastance and resistance. New results were displayed on the screen about every minute. The automated method was first tested in a series of 18 guinea-pigs; the respiratory parameters were compared with those obtained by the occlusion method proposed by Rossi et al. (J Appl Physiol, 58: 1849, 1985). They were found not significantly different and very strongly correlated (p less than 0.001). The ability of the constant flow method to detect changes in respiratory mechanics was then tested in a series of nine patients, after anaesthetic induction. The results obtained were in accordance with those previously published: a rise in both respiratory elastance and resistance. After giving 1 mg atropine intravenously, the respiratory resistance fell rapidly over a 5 min period, and then reached a plateau. The constant flow method, which avoids interruption in the mechanical ventilation and is sensitive to small changes in respiratory parameters, appears particularly convenient for the peroperative monitoring of patients.

Airway Resistance↗

Comparative effects of bisoprolol and acebutolol in smokers with airway obstruction.

1. The effects of single oral doses of 10 mg bisoprolol and 400 mg acebutolol on respiratory function were studied in nine smokers with airway obstruction in a double-blind, placebo-controlled experiment. 2. The effects of the drugs were assessed by measuring specific airway conductance (sGaw) for 3 h after their administration and by studying their interaction with the bronchodilator response to inhaled salbutamol. 3. sGaw did not change for 3 h after bisoprolol or acebutolol administration. The bronchodilator response to inhaled salbutamol was not affected by bisoprolol but significantly reduced by acebutolol (P less than 0.05 vs placebo). 4. Under these conditions, bisoprolol behaves like a selective beta 1-adrenoceptor antagonist but acebutolol exhibits less beta 1-adrenoceptor selectivity.

Acebutolol↗

Low VA/Q areas: arterial-alveolar N2 difference and multiple inert gas elimination technique.

In 16 critically ill patients the arterial-alveolar N2 difference and data from the multiple inert gas elimination technique (MIGET) were compared in the evaluation of the contribution of low alveolar ventilation-perfusion ratio (VA/Q) lung regions (0.005 less than VA/Q less than 0.1) to venous admixture (Qva/QT). The arterial-alveolar N2 difference was determined using a manometric technique for the measurement of the arterial N2 partial pressure (PN2). We adopted a two-compartment model of the lung, one compartment having a VA/Q of approximately 1, the other being open, gas filled, unventilated (VA/Q = 0), and in equilibrium with the mixed venous blood. This theoretical single compartment represents all lung regions responsible for the arterial-alveolar N2 difference. The fractional blood flow to this compartment was calculated using an appropriate mixing equation (Q0/QT). There was a weak but significant relationship between Q0/QT and the perfusion fraction to lung regions with low VA/Q (0.005 less than VA/Q less than 0.1) (r = 0.542, P less than 0.05) and a close relationship between Q0/QT and the perfusion fraction to lung regions with VA/Q ratios less than 0.9 (r = 0.862, P less than 0.001) as obtained from MIGET. The difference Qva/QT-Q0/QT yielded a close estimation of the MIGET right-to-left shunt (Qs/QT) (r = 0.962, P less than 0.001). We conclude that the assessment of the arterial-alveolar N2 difference and Q0/QT does not yield a quantitative estimation of the contribution of pathologically low VA/Q areas to QVa/QT because these parameters reflect an unknown combination of pathological and normal (0.1 less than VA/Q less than 0.9) gas exchange units.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Gas Analysis↗

Interpretation of the krypton-81m dynamic series: the distribution of a tidal breath.

Lung scans during cyclic breathing of krypton-81m, an isotope with a 13-s half-life, were acquired in "list mode," where both temporal and spatial information are preserved. Subjects in the left lateral decubitus position breathed with two tidal volumes at each of two frequencies. Profiles of total activity over the acquisition period were examined. They showed little effect of frequency or tidal volume on the distribution of air between dependent and non-dependent regions. Dynamic series for ensemble-averaged breaths were constructed. The regional flow per unit volume was shown to correspond to the time derivative of the regional activity of the dynamic series divided by the corresponding activity. Both the relative timing of the gas flow to different lung regions and the flow per unit volume as a function of time were obtained from the dynamic series. The dependent lung was seen to be better ventilated throughout the respiratory cycle except for brief periods at the start of inspiration and the end of expiration. Most of the dead-space gas can be construed to enter and leave the dependent lung.

Female↗

Inspiratory work of breathing during spontaneous ventilation using demand valves and continuous flow systems.

To diminish the work of breathing, some demand valve systems are equipped with inspiratory pressure support (IPS). The purpose of this study was to evaluate the work performed during spontaneous breathing using the Siemens Servo 900C ventilator (SVC) at the minimal IPS level available, and comparing it with a demand valve ventilator without IPS, the Ohmeda CPU1 (CPU1), and with a home-built continuous flow system (CFS). We found a larger minute ventilation and inspiratory peak flow with the SVC and the CFS than with the CPU1 (p less than 0.05). When the work of breathing was measured at the airway opening, we found that the CFS led to the least amount of work (0.17 +/- 0.05 J.L-1, p less than 0.05). Additionally, this work was strikingly less for SVC than for CPU1 (0.22 +/- 0.06 versus 0.42 +/- 0.10 J.L-1, p less than 0.001) as a result of a higher flow supplied by the SVC. By contrast, the work measured using the esophageal pressure, i.e., including the work dissipated on the lung and airways, was significantly reduced with the CFS (1.34 +/- 0.45 J.L-1, p less than 0.05), but surprisingly not different between SVC and CPU1 (1.49 +/- 0.57 versus 1.54 +/- 0.51 J.L-1). We conclude that the absence of a demand valve in CFS involves the lowest work of breathing. Likewise, the high flow capability in SVC reduces the work necessary to overcome the circuit and demand valve resistances.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of cardioselective beta blockade on the peripheral lung in guinea pigs.

Impairment of lung function with selective beta-1 blocking drugs has been repeatedly demonstrated in guinea pigs, normal subjects and asthmatic patients. The effects of several beta blockers, propranolol (non-selective), atenolol (beta-1 selective), IPS 339 (beta-2 selective) on histamine-induced bronchoconstriction have been investigated in 30 anaesthetized and mechanically ventilated guinea pigs, measuring changes in conductance and dynamic compliance. Their effects on peripheral lung, where only beta-2 adrenoceptors are present, were more specifically assessed using changes in lung distensibility by means of static pressure-volume curves. Atenolol (1 mg.kg-1), IPS 339 (2 mg.kg-1) and propranolol (2 mg.kg-1) enhanced histamine-induced decrease in lung distensibility, conductance and dynamic compliance. The decrease was of the same order of magnitude for all three parameters. Atenolol (1 mg.kg-1) and propranolol (2 mg.kg-1) decreased lung distensibility to the same extent. By contrast low dose atenolol (0.1 mg.kg-1) did not potentiate histamine-induced bronchoconstriction although this dose did produce a significant cardiac beta blockade. These results demonstrate that 1) beta blockers have a clear effect on the peripheral lung, 2) beta-1 adrenoceptors are not involved in pulmonary effects of cardioselective drugs. They suggest that dose dependent loss of selectivity is the major mechanism behind impairment of lung function following such drugs.

Adrenergic beta-Antagonists↗

Mechanism of histamine-induced epinephrine release in guinea pig.

The aims of this study were to provide direct evidence that in anesthetized guinea pigs i.v. administration of histamine induces sympathoadrenal activation and to identify the source and mechanism of histamine-induced epinephrine release. Plasma epinephrine measurements were used as the index of sympathoadrenal activity. In intact guinea pigs, histamine infusion caused a 3-fold rise in plasma epinephrine levels. In guinea pigs pretreated with 6-hydroxydopamine to obtain chemical sympathectomy, the rise in plasma epinephrine induced by histamine was distinctly smaller than in controls. This rise was completely inhibited in guinea pigs pretreated with the ganglion blocking agent hexamethonium and in pithed guinea pigs. Pretreatment with the H2-receptor antagonist cimetidine or the H1-receptor antagonist mepyramine reduced the rise in plasma epinephrine. These results demonstrate that in guinea pigs, epinephrine is released not only from the adrenal medulla but also from nerve endings and that histamine releases epinephrine by indirect action through central reflex pathways.

Animals↗

Comparison of the dose-response curves obtained by forced oscillation and plethysmography during carbachol inhalation.

We compared the cumulative dose-response curves obtained during carbachol inhalation by simultaneous measurements of airway specific conductance (sGaw) and respiratory conductance, in 23 subjects with or without bronchial hyperresponsiveness. The sGaw was measured by a body plethysmograph, whilst the random noise forced oscillation technique (FOT) was used to determine respiratory conductance. The sGaw was compared to respiratory conductance extrapolated to zero frequency (Grs0). Bronchial sensitivity was assessed by the threshold dose of carbachol (TD) that induced a decrease in sGaw and Grs0 of twice the baseline coefficient of variation. Bronchial responsiveness was assessed by the slopes (S) of the individual dose-response curves. The TD and S values obtained by FOT and by plethysmography were closely correlated (p less than 0.001). The carbachol doses inducing a 50% reduction in sGaw were equivalent to those causing a 42% reduction in Grs0 (r = 0.90; p less than 0.001). During bronchial challenge testing, FOT provides comparable information in terms of bronchial sensitivity and responsiveness to that supplied by plethysmography.

Adult↗

[Calculation of the ventilation-perfusion ratio in the scintigraphic diagnosis of pulmonary embolism].

Ventilation perfusion scanning fails to diagnose pulmonary embolism in matched defects. In 61 patients (19 with pulmonary embolism proved by angiography, 32 with chronic obstructive lung disease and 10 with acute bacterial pneumonia) we computed the ventilation perfusion ratio (V/Q) in these matched defects, using Krypton 81 m. This analysis demonstrated that the diagnosis of pulmonary embolism could be made with a specificity of 100% when the V/Q ratio was greater than 1.2 in the matched defects. Pulmonary embolism was characterized by a perfusion defect with a high V/Q ratio, even in Laennec infarction. In contrast, the analysis excluded the diagnosis of pulmonary embolism and suggested another disease when the V/Q was less than 0.95 with a specificity of 95%. Perfusion defects in acute pneumonia always had a V/Q less than 1. The diagnosis remained difficult in chronic obstructive lung disease when pulmonary embolism was suspected on subsegmental defects. Nevertheless this could be solved in about 50% of the cases by quantitative analysis. We feel, therefore, that ventilation perfusion scanning should be quantified by V/Q analysis to improve the diagnosis of pulmonary embolism.

Adult↗

Effect of low-level NO2 chronic exposure on elastase-induced emphysema.

The effect of chronic exposure to 2 ppm nitrogen dioxide (NO2) for 8 hr a day, 5 days a week, for 8 weeks was assessed in normal and emphysematous hamsters by measuring (1) lung morphometry (mean linear intercept [Lm] and internal surface area [ISA]), (2) lung mechanics (lung volume, compliance and coefficient of static deflation, pressure-volume curve fitted to an exponential equation), and (3) serum elastolytic activity and protease inhibitor capacity. Emphysema was induced by a single intratracheal injection of 6 IU porcine pancreatic elastase. Four groups of animals were used; Control, NO2-exposed, elastase-treated, and NO2-exposed postelastase. Our results show that NO2 exposure alone induced mild emphysematous lesions whose degree of severity estimated by morphometry increase in Lm and decrease in ISA. P less than 0.01) was of the same order as that of the lesions induced by 6 IU elastase. Exposure to 2 ppm NO2 enhanced elastase-induced emphysema (further increased Lm and further reduced ISA. P less than 0.01). By contrast, study of lung mechanics revealed no difference between the control and NO2-exposed groups or between the elastase-treated animals exposed to NO2 and those not so exposed. This apparent discrepancy between results of morphometry and lung mechanics may be due to the lower sensitivity of lung mechanics parameters and their consequent inability to reflect changes in the emphysematous lesions induced by elastase injection or 2 ppm NO2 inhalation. In vivo, serum elastolytic activity and protease inhibitor capacity were not modified in any group, indicating that either serum does not reflect the degree of protease inhibitor capacity in the alveolar spaces or chronic inhalation of low concentrations of NO2 is not sufficient to cause elastase/antielastase imbalance. Lastly, our results suggest that chronic exposure to 2 ppm NO2 may cause individuals with inherited or acquired emphysematous lesions to develop more severe emphysema.

Animals↗

Failure of enhancement by labetalol of bronchopulmonary effects of histamine in guinea-pigs: independence of alpha-adrenoceptor antagonism.

The effect of labetalol on histamine-induced bronchoconstriction was studied in anaesthetized guinea-pigs. Unlike propranolol (1 mg kg-1), the same dose of labetalol did not enhance histamine-induced bronchoconstriction. To determine whether the absence of enhancement of the respiratory effects of histamine by labetalol was due to its alpha 1-blocking properties or to its partial agonist activity at beta 2-adrenoceptors, the effects of propranolol plus prazosin and of propranolol plus labetalol on histamine-induced bronchoconstriction were examined. In both cases, the bronchoconstrictor effects of histamine were enhanced to the same extent as with propranolol alone. These data support the hypothesis that the non impairment of respiratory mechanics by labetalol is not due to antagonism at alpha-adrenoceptors and may be mediated by its partial agonist activity at beta 2-adrenoceptors.

Adrenergic alpha-Antagonists↗

High frequency chest wall oscillation in patients with chronic air-flow obstruction.

In order to assess high frequency chest wall oscillation (HFCWO) as a way to assist spontaneous breathing in obstructive lung disease, we studied 12 patients with severe and stable COPD. HFCWO at 5 Hz were applied by means of an inflatable vest. In order to avoid any discomfort, oscillations were applied only during the expiratory phase of the spontaneous breathing cycle. We compared gas exchange and pattern of breathing during control and HFCWO periods, each lasting 15 min. Minute ventilation did not change, but the pattern of breathing was markedly altered during HFCWO: breathing frequency decreased (p less than 0.001) from 18 +/- 6/min during control to 14 +/- 5/min, whereas tidal volume increased (p less than 0.01) from 600 +/- 200 ml during control to 860 +/- 400 ml. Secondary to this change in the pattern of breathing, arterial PO2 increased slightly (p less than 0.01) from 54 +/- 7 mm Hg during control to 57 +/- 8 mm Hg during HFCWO, and arterial PCO2 significantly (p less than 0.01) decreased from 46 +/- 6 mm Hg during control to 43 +/- 7 mm Hg during HFCWO. In addition, duty cycle (Ti/Ttot) decreased (p less than 0.001) from 0.37 +/- 0.03 s during control to 0.29 +/- 0.05 s during HFCWO. Such a decrease in duty cycle suggest that inspiratory muscle work was facilitated under HFCWO. In 8 patients, we obtained the tension-time index (TTdi), or the product of duty cycle and Pdi/Pdimax, and found that this index significantly decreased (p less than 0.05) from 0.06 +/- 0.03 during control to 0.04 +/- 0.02 during HFCWO.(ABSTRACT TRUNCATED AT 250 WORDS)

Dyspnea↗

Density and frequency dependence of resistance in early airway obstruction.

The forced oscillation technique is a noninvasive and effort-independent test used to characterize the mechanical impedance of the respiratory system. The aim of this study was to assess the sensitivity of this method in detecting early airway abnormalities caused by smoking or occupational hazards. Respiratory mechanical parameters by the forced oscillation technique and maximal expiratory flow volume (MEFV) curves were obtained in a group of 82 workers from a gas manufacturing plant. In addition, the variations in the frequency dependence of total respiratory resistance between air breathing and a mixture of helium-oxygen (He-O2) were measured. All parameters were normalized for age, height, and weight. In order to compare the 2 types of testing, multiple linear regressions were performed with smoking or exposure as independent variables on one hand and parameters of the 2 types of testing on the other hand. This statistical procedure showed that 2 parameters of the forced oscillation technique constantly reached higher levels of significance than those of the MEFV parameters in the regression equations describing smoking history and occupational exposure: these were the frequency dependence of resistance and the change in frequency dependence between air and He-O2 breathing. When nonsmokers, ex-smokers, and smokers were considered separately, the degree of frequency dependence of resistance and the change in frequency dependence between air and He-O2 breathing were the only parameters that were significantly different between these 3 groups (one-way analysis of variance).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Real-time detection of ventilatory maneuvers by a microcomputer.

The SYTER software system was built around an Apple II microcomputer to automatically process the data yielded by three ventilatory tests: analysis of lung elasticity during an expiratory maneuver, plethysmographic measurement of airway resistance during a panting maneuver, and similar measurements of lung volumes. A volume signal is displayed to the operator throughout each test to help control the maneuver. The various stages of the test are recognized in real time by routines written in assembling language, so that significant data are displayed and stored during the maneuver. This paper describes the algorithms used to perform waveform analysis, and presents illustrative displays obtained in the Lung Function Laboratory.

Airway Resistance↗

Dependence of central airway resistance on frequency and tidal volume: a model study.

The resistance of a hollow cast of human central airways was measured during true sinusoidal airflow oscillations over a wide range of frequencies (0.5-40 Hz) and for various flow amplitudes up to 8 l/s. Pressure and flow were measured in the trachea with high-performance transducers, digitized and averaged over 100 cycles. Data were studied at two points in the flow cycle: at peak inspiratory and expiratory flows and in the two neighborhoods around zero flow where airway resistance (Rv approximately equal to o) was taken as the average slope of the pressure-flow (P-V) curve in each zone. When data obtained near peak flow were plotted in terms of dimensionless pressure drop vs. peak Reynolds number (Rem) and compared with steady-state data, we found no difference up to 2 Hz as previously reported (Isabey and Chang, J. Appl. Physiol. 51: 1338-1348, 1981), a slight decay in pressure drop between 4 and 8 Hz, a frequency-dependent increase in peak flow resistance at high frequencies (10-40 Hz) governed by the Strouhal number alpha 2/Rem beyond alpha 2/Rem = 0.5. On the other hand RV approximately equal to o was found to increase relative to steady state as local acceleration increases, e.g., as peak flow increases at a fixed frequency; this differs from the classical linear theory of oscillatory flow in a long straight tube. To explain these results, we had to use, as in our previous study, an alternative expression for the Strouhal number, i.e., epsilon = L X A X (dV/dt)/V2 (where L and A are the length and cross-sectional area of the trachea and V is a constant flow range over which resistance around flow reversal was computed), which accurately reflects the ratio of local acceleration [d(V/A)/dt)] to convective acceleration [(V/A)2/L] in developing branching flow. Finally, to delineate the regions of dominance of each of the dimensionless parameters, we compiled frequency-tidal volume diagrams for peak flows as well as for reversal. Epsilon, which is negligible near peak flows, appeared to govern the oscillatory P-V relationship near flow reversal in a transitional region of the diagram located between regions of steadiness, or moderate unsteadiness, and a region of dominant unsteadiness governed by alpha.

Airway Resistance↗

Respiratory resistance with histamine challenge by single-breath and forced oscillation methods.

Relaxed expirations were obtained from five anesthetized dogs under control conditions and during various rates of intravenous infusion of histamine. All volume vs. time curves obtained from 20 ms to 2 s after the start of expiration were poorly described by a single exponential function but were fitted very well by a biexponential function. The resistance of the respiratory system as a function of frequency from 2 to 26 Hz was also determined by the forced oscillation method in the same dogs. Three two-compartment models of the respiratory system were identified from the exponentials fitted to the relaxed expiration data, and the one that had the most plausible parameter values under control conditions consisted of a homogeneous lung compartment connected to a viscoelastic compartment. Although a two-compartment model is arguably appropriate for describing relaxed expirations in normal dogs, physiological considerations suggest that there should be more than two interacting components with histamine infusion. We cannot identify all these components from our data, however. The equivalent complex impedance of the respiratory system was also calculated from the biexponential curves and showed significant variation in resistance over the frequency range from 0 to 2 Hz and negligible variation above 2 Hz. The calculated resistances at 2 Hz were consistently higher than those obtained by the forced oscillation method, which may be due to the nonlinear behavior of the respiratory system during relaxed expiration. We conclude that the single-breath and forced oscillation methods should be viewed as providing complimentary information about respiratory resistance.

Airway Resistance↗