Validation of esophageal balloon technique at different lung volumes and postures

1987 ◽  
Vol 62 (1) ◽  
pp. 315-321 ◽  
Author(s):  
A. Baydur ◽  
E. J. Cha ◽  
C. S. Sassoon

The esophageal balloon technique for measuring pleural surface pressure (Ppl) has recently been shown to be valid in recumbent positions. Questions remain regarding its validity at lung volumes higher and lower than normally observed in upright and horizontal postures, respectively. We therefore evaluated it further in 10 normal subjects, seated and supine, by measuring the ratio of esophageal to mouth pressure changes (delta Pes/delta Pm) during Mueller, Valsalva, and occlusion test maneuvers at FRC, 20, 40, 60, and 80% VC with the balloon placed 5, 10, and 15 cm above the cardia. In general, delta Pes/delta Pm was highest at the 5-cm level, during Mueller maneuvers and occlusion tests, regardless of posture or lung volume (mean range 1.00–1.08). At 10 and 15 cm, there was a progressive increase in delta Pes/delta Pm with volume (from 0.85 to 1.14). During Valsalva maneuvers, delta Pes/delta Pm also tended to increase with volume while supine (range 0.91–1.04), but was not volume-dependent while seated. Qualitatively, observed delta Pes/delta Pm fit predicted corresponding values (based on lung and upper airway compliances). Quantitatively there were discrepancies probably due to lack of measurement of esophageal elastance and to inhomogeneities in delta Ppl. At every lung volume in both postures, there was at least one esophageal site where delta Pes/delta Pm was within 10% of unity.

1998 ◽  
Vol 84 (5) ◽  
pp. 1639-1645 ◽  
Author(s):  
Maurice Beaumont ◽  
Redouane Fodil ◽  
Daniel Isabey ◽  
Frédéric Lofaso ◽  
Dominique Touchard ◽  
...  

We measured upper airway caliber and lung volumes in six normal subjects in the sitting and supine positions during 20-s periods in normogravity, hypergravity [1.8 + head-to-foot acceleration (Gz)], and microgravity (∼0 Gz) induced by parabolic flights. Airway caliber and lung volumes were inferred by the acoustic reflection method and inductance plethysmography, respectively. In subjects in the sitting position, an increase in gravity from 0 to 1.8 +Gz was associated with increases in the calibers of the retrobasitongue and palatopharyngeal regions (+20 and +30%, respectively) and with a concomitant 0.5-liter increase in end-expiratory lung volume (functional residual capacity, FRC). In subjects in the supine position, no changes in the areas of these regions were observed, despite significant decreases in FRC from microgravity to normogravity (−0.6 liter) and from microgravity to hypergravity (−0.5 liter). Laryngeal narrowing also occurred in both positions (about −15%) when gravity increased from 0 to 1.8 +Gz. We concluded that variation in lung volume is insufficient to explain all upper airway caliber variation but that direct gravity effects on tissues surrounding the upper airway should be taken into account.


1990 ◽  
Vol 68 (5) ◽  
pp. 2159-2164 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
M. Desmeules

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.


1993 ◽  
Vol 74 (3) ◽  
pp. 1039-1044 ◽  
Author(s):  
R. Peslin ◽  
D. Navajas ◽  
M. Rotger ◽  
R. Farre

The reliability of the esophageal balloon technique in measuring high-frequency changes in pleural pressure (Ppl) was investigated in six normal subjects by studying the amplitude ratio (A) and phase angle (phi) of esophageal (Pes) and mouth (Pm) pressures during airway occlusion and while pseudorandom pressure variations (2–32 Hz) were applied to the chest. The measurements were made with a common esophageal balloon-catheter system connected to a high-impedance piezoresistive transducer. When the cheeks were firmly supported, A averaged 1.08 +/- 0.063 at 2 Hz and 1.06 +/- 0.11 at 32 Hz. Pes increasingly led Pm with increasing frequency, and phi averaged 20.8 +/- 4.0 degrees at 32 Hz. Washing the airways with 80% He-20% O2 reduced phi by 50%. When the cheeks were not supported, A exhibited a strong positive frequency dependence, averaging 1.71 +/- 0.34 at 32 Hz, whereas phi increased much faster below 20 Hz and tended to decrease afterward. Because the esophageal transfer function Pes/Ppl = (Pes/Pm)/(Ppl/Pm), we could estimate Pes/Ppl by computing for individual subjects the pressure difference between the pleura and the mouth based on the lung and upper airway wall properties that were measured separately. The results suggest that the ratio of Pes and Ppl remains close to unity from 2 to 32 Hz, but Pes lags slightly behind Ppl (phi equals about -7 degrees at 32 Hz).


1981 ◽  
Vol 50 (3) ◽  
pp. 650-657 ◽  
Author(s):  
N. J. Douglas ◽  
G. B. Drummond ◽  
M. F. Sudlow

In six normal subjects forced expiratory flow rates increased progressively with increasing degrees of chest strapping. In nine normal subjects forced expiratory flow rates increased with the time spent breathing with expiratory reserve volume 0.5 liters above residual volume, the increase being significant by 30 s (P less than 0.01), and flow rates were still increasing at 2 min, the longest time the subjects could breathe at this lung volume. The increase in flow after low lung volume breathing (LLVB) was similar to that produced by strapping. The effect of LLVB was diminished by the inhalation of the atropinelike drug ipratropium. Quasistatic recoil pressures were higher following strapping and LLVB than on partial or maximal expiration, but the rise in recoil pressure was insufficient to account for all the observed increased in maximum flow. We suggest that the effects of chest strapping are due to LLVB and that both cause bronchodilatation.


1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.


1992 ◽  
Vol 73 (6) ◽  
pp. 2373-2381 ◽  
Author(s):  
S. J. Cala ◽  
J. Edyvean ◽  
L. A. Engel

We measured the electromyographic (EMG) activity in four chest wall and trunk (CWT) muscles, the erector spinae, latissimus dorsi, pectoralis major, and trapezius, together with the parasternal, in four normal subjects during graded inspiratory efforts against an occlusion in both upright and seated postures. We also measured CWT EMGs in six seated subjects during inspiratory resistive loading at high and low tidal volumes [1,280 +/- 80 (SE) and 920 +/- 60 ml, respectively]. With one exception, CWT EMG increased as a function of inspiratory pressure generated (Pmus) at all lung volumes in both postures, with no systematic difference in recruitment between CWT and parasternal muscles as a function of Pmus. At any given lung volume there was no consistent difference in CWT EMG at a given Pmus between the two postures (P > 0.09). However, at a given Pmus during both graded inspiratory efforts and inspiratory resistive loading, EMGs of all muscles increased with lung volume, with greater volume dependence in the upright posture (P < 0.02). The results suggest that during inspiratory efforts, CWT muscles contribute to the generation of inspiratory pressure. The CWT muscles may act as fixators opposing deflationary forces transmitted to the vertebral column by rib cage articulations, a function that may be less effective at high lung volumes if the direction of the muscular insertions is altered disadvantageously.


2001 ◽  
Vol 90 (4) ◽  
pp. 1441-1446 ◽  
Author(s):  
Mario Filippelli ◽  
Riccardo Pellegrino ◽  
Iacopo Iandelli ◽  
Gianni Misuri ◽  
Joseph R. Rodarte ◽  
...  

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.


1979 ◽  
Vol 47 (2) ◽  
pp. 319-324 ◽  
Author(s):  
C. J. Martin ◽  
S. Das ◽  
A. C. Young

The “anatomical” dead space is commonly measured by sampling an inert gas (N2) and volume in the exhalation following a large breath of oxygen (VD(F)). It may also be measured from an inert gas washout (VD(O)) that describes both volume and the delivery of VD(O) throughout the expiration. VD(O) is known to increase with age and is enlarged in some obstructive syndromes. VD(O) was appreciably larger than VD(F) in our normal subjects. Both measures increased with lung volume, the increase being entirely due to an increase in the volume of phase I. Physiological dead space (VD(p)) however, did not change significantly with lung volume, showing “alveolar” dead space to diminish as a result. An increase in VD(O) occurred with increasing respiratory frequency that was explained by the increase in volume of phase I. Although an increase in VD(F) occurred with frequency, this was significantly less than that seen by VD(O), i.e., VD(F) did not see the progressive increase in phase I volume with frequency. No lung volume or frequency changes, parasympatholytic or sympathomimetic drugs, or altered patterns of breathing simulated the late delivery of dead space seen in age and some obstructive syndromes.


1982 ◽  
Vol 53 (3) ◽  
pp. 698-702 ◽  
Author(s):  
P. Helms

In 57 infants and very young children, less than 2 yr of age and with a variety of cardiopulmonary illnesses, problems were encountered in the estimation of lung volume with the plethysmographic technique. In 19 subjects calculated thoracic gas volume (TGV) was found to be consistently larger when airway occlusions were performed at low lung volumes than when performed at higher lung volumes. In 13 infants, changes in intraesophageal pressure (Pes) during airway occlusions were found to be larger than simultaneous changes in mouth pressure. In 25 subjects in whom none of the above changes were observed, total pulmonary resistance (TPR) and airway resistance (Raw) did not differ significantly [mean TPR, 50.1 +/- 27.5 cmH2O X l-1; mean Raw, 48.1 +/- 26.5 (P greater than 0.5)]. In the 13 subjects in whom the delta Pes-to-delta Pm occlusion ratio exceeded 1.05, closest agreement with specific resistance (sRaw) and TPR derived lung volume was found when TGV was calculated with delta Pes rather than mouth pressure change (delta Pm). A similar close agreement with the sRaw TPR derived volume was obtained when TGV was calculated during airway occlusions at the higher lung volume. Two separate lung models are proposed to explain these observations, one with a segmental airway closure and the other with more a generalized airway closure. If plethysmographic techniques are to be used in these young subjects for the estimation of lung volume and airway resistance, possible errors may be reduced by performing airway occlusions at lung volumes above functional residual capacity and noting the delta Pes-to-delta Pm ratio obtained during the occlusion.


1981 ◽  
Vol 60 (5) ◽  
pp. 513-518 ◽  
Author(s):  
S. C. Gandevia ◽  
K. J. Killian ◽  
E. J. M. Campbell

1. With standard psychophysical techniques the ability of normal subjects to detect negative pressures applied at the mouth was estimated. 2. The ability to detect changes in pressure when confined to the upper airway by closure of the glottis was less than when the pressures were transmitted below the glottis and were actively overcome by inspiratory muscle contraction. 3. The ability to detect changes in pressure with the glottis open was also impaired by passive ventilation and vibration of the chest. 4. Our results imply that the most sensitive mechanism for the detection of negative pressures applied at the mouth involves afferent information from active inspiratory muscle contraction.


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