A method for the assessment of phasic vagal influence on tidal volume

1975 ◽  
Vol 38 (2) ◽  
pp. 335-343 ◽  
Author(s):  
M. Younes ◽  
S. Iscoe ◽  
J. Milic-Emili
Keyword(s):  
Tidal Volume ◽  
Respiratory System ◽  
Spontaneous Breathing ◽  
Volume Changes ◽  
Lung Volumes ◽  
Lung Inflation ◽  
Airway Occlusion ◽  
Tracheal Pressure ◽  
Vagal Cooling ◽  
Vagal Influence

Vagal influence related to lung volume changes results in reduction in tidal volume during spontaneous breathing due primarily to premature termination of inspiration. The strength of this vagal influence was traditionally assessed by the duration of apnea following lung inflation, a method recently shown to be inadequate and potentially misleading. An alternate method is described utilizing analysis of the volume tracing of spontaneous breaths and the tracheal pressure tracing during the first breath following airway occlusion at FRC. A formula was devised which, on the basis of previous observations, should predict the tidal volume to be obtained in the absence of phasic vagal influence. The formula was tested in four pentobarbital-anesthetized rabbits using a technique of vagal cooling which rapidly eliminated the vagal influence under study. It was found that the tidal volume obtained following vagal block could be accurately predicted provided allowances were made for the vagally mediated terminal inhibition during spontaneous breathing and the relative stiffness of the respiratory system at high lung volumes.

Augmentation of phrenic neural activity by increased rates of lung inflation

1981 ◽  
Vol 50 (1) ◽  
pp. 149-161 ◽  
Author(s):  
A. I. Pack ◽  
R. G. DeLaney ◽  
A. P. Fishman
Keyword(s):  
Tidal Volume ◽  
Volume Change ◽  
Neural Activity ◽  
Negative Pressure ◽  
Spontaneous Breathing ◽  
Moving Average ◽  
Constant Flow ◽  
Lung Inflation ◽  
Negative Pressure Ventilation ◽  
Single Breath

Studies were conducted in anesthetized paralyzed dogs using a cycle-triggered constant-flow ventilator, which ventilated the animal in phase with the recorded phrenic neural activity. Intermittently tests were performed in which the animal was ventilated with a different airflow for a single breath. Increased airflows, within the range generated during spontaneous breathing, caused an increased rate of rise of the moving average phrenic neurogram and a shortening of the duration of the nerve burst. The magnitude of the increase in the rate of rise of the neurogram was related to the level of inspiratory airflow. Tests with brief pulses of airflow showed that an increase in the rate of rise of the phrenic neurogram could be produced without inflating the lung above the resting tidal volume of the animal. Similar results were obtained with negative-pressure ventilation and the effects were abolished by vagotomy. This vagally mediated augmentation of phrenic neural output may accelerate the inspiratory volume change in the lung during spontaneous breathing at hyperpneic levels.

Effect of changes in lung volume on respiratory system compliance in newborn infants

1989 ◽  
Vol 67 (3) ◽  
pp. 1192-1197 ◽  
Author(s):  
F. Ratjen ◽  
R. Zinman ◽  
A. R. Stark ◽  
L. E. Leszczynski ◽  
M. E. Wohl
Keyword(s):  
Tidal Volume ◽  
Respiratory System ◽  
Lung Volume ◽  
Newborn Infants ◽  
Face Mask ◽  
Flow Volume ◽  
Respiratory System Compliance ◽  
Tidal Breathing ◽  
Volume Changes ◽  
Passive Flow

Total respiratory system compliance (Crs) at volumes above the tidal volume (VT) was studied by use of the expiratory volume clamping (EVC) technique in 10 healthy sleeping unsedated newborn infants. Flow was measured with a pneumotachograph attached to a face mask and integrated to yield volume. Volume changes were confirmed by respiratory inductance plethysmography. Crs measured by EVC was compared with Crs during tidal breathing determined by the passive flow-volume (PFV) technique. Volume increases of approximately 75% VT were achieved with three to eight inspiratory efforts during expiratory occlusions. Crs above VT was consistently greater than during tidal breathing (P less than 0.0005). This increase in Crs likely reflects recruitment of lung units that are closed or atelectatic in the VT range. Within the VT range, Crs measured by PFV was compared with that obtained by the multiple-occlusion method (MO). PFV yielded greater values of Crs than MO (P less than 0.01). This may be due to braking of expiratory airflow after the release of an occlusion or nonlinearity of Crs. Thus both volume recruitment and airflow retardation may affect the measurement of Crs in unsedated newborn infants.

Decay of inspiratory muscle pressure during expiration in anesthetized cats

1983 ◽  
Vol 54 (2) ◽  
pp. 408-413 ◽  
Author(s):  
W. A. Zin ◽  
L. D. Pengelly ◽  
J. Milic-Emili
Keyword(s):  
Respiratory System ◽  
Time Course ◽  
Pentobarbital Sodium ◽  
Airway Occlusion ◽  
Inspiratory Muscles ◽  
Tracheal Pressure ◽  
Resistive Loads ◽  
The Moment ◽  
Spontaneously Breathing

In six spontaneously breathing anesthetized cats (pentobarbital sodium, 35 mg/kg) we studied the antagonistic pressure developed by the inspiratory muscles during expiration (PmusI). This was accomplished in two ways: 1) with our previously reported method (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 52: 1266–1271, 1982) based on the measurement of changes in lung volume and airflow during spontaneous expiration, together with determination of the total passive respiratory system elastance and resistance; and 2) measurement of the time course of changes in tracheal/pressure after airway occlusion at end inspiration, up to the moment when the inspiratory muscles become completely relaxed. The agreement between the two methods is generally good, both in the amplitude of PmusI and in its time course. We also applied the first method to spontaneous expirations through added linear resistive loads. These did not alter the relative decay of PmusI. Thus in anesthetized cats the braking action of the inspiratory muscles does not decrease when expiratory resistive loads are added, i.e., when such braking is clearly not required.

Phasic vagal influence on inspiratory motor output in anesthetized human subjects

1980 ◽  
Vol 49 (4) ◽  
pp. 609-619 ◽  
Author(s):  
J. Polacheck ◽  
R. Strong ◽  
J. Arens ◽  
C. Davies ◽  
I. Metcalf ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Human Subjects ◽  
Normal Subjects ◽  
Airway Disease ◽  
Apparent Volume ◽  
Motor Output ◽  
Restrictive Lung Disease ◽  
Tracheal Pressure ◽  
Inspiratory Motor ◽  
Vagal Influence

Vagal influence on inspiratory motor output was assessed in 20 normal subjects and in 12 patients with respiratory disorders under enflurane anethesia using the method of airway occlusion. The change in inspiratory duration during occlusion (delta TI) was measured from mechanical parameters (respiratory flow and tracheal pressure). In eight of the subjects, however, the effect of occlusion and augmentation of tidal volume was further evaluated from diaphragmatic electromyogram. In normal subjects delta TI (mechanical) averaged 0.15 s (range -0.1 to +0.77 s) and correlated with the duration of inspiration during occlusion. Electromyographic observations indicated that the change in neural TI exceeds the change in mechanical TI by approximately 0.2 s and that augmentation of tidal volume shortens TI with no apparent volume threshold. There was a tendency for vagal influence to be higher with restrictive lung disease and lower with obstructive airway disease. These observations indicate that a majority of humans display a significant vagal influence on TI in the spontaneous tidal volume range under anesthesia.

Mechanical aspects of chest wall distortion

1985 ◽  
Vol 59 (2) ◽  
pp. 295-304 ◽  
Author(s):  
J. P. Mortola ◽  
M. Saetta ◽  
G. Fox ◽  
B. Smith ◽  
S. Weeks
Keyword(s):  
Tidal Volume ◽  
Respiratory System ◽  
Volume Change ◽  
Spontaneous Breathing ◽  
Relaxation Curve ◽  
Abdominal Pressure ◽  
Human Infants ◽  
Adult Rats ◽  
Inspiratory Muscles ◽  
Phrenic Stimulation

During passive inflation of the respiratory system, the rib cage (RC) expands because the pressure applied to it [approximately equal to abdominal pressure (Pab)] increases. Similar Pab-tidal volume (VT) relationships between passive and spontaneous inspirations would occur only if 1) Pab acts on RC equally in the two situations (no distortion) or 2) the extradiaphragmatic inspiratory muscles expand RC, compensating for distortion. In anesthetized adult rats and in sleeping human infants the passive relationships between VT and Pab or abdomen motion (AB) were constructed by occluding the airways during expiration. For a given Pab (or AB) in active breathing VT averaged 55% (rats) and 49% (infants) of the passive volume change. With phrenic stimulation in rats VT was only slightly less than during spontaneous breathing, indicating that, in the latter case, the respiratory system was essentially driven only by the diaphragm. In both species occasional breaths with large RC expansion occurred, and VT was then equal to or larger than the passive volume at iso-Pab. We conclude that 1) RC distortion decreases VT to approximately half of the passive value and 2) being on the relaxation curve reflects “compensated” distortion and not absence of it.

Effects of hypercapnia on Breuer-Hering threshold for inspiratory termination

1984 ◽  
Vol 57 (4) ◽  
pp. 1211-1221 ◽  
Author(s):  
T. L. Clanton ◽  
W. T. Lipscomb
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
Neural Mechanism ◽  
Co2 Concentration ◽  
Lung Volumes ◽  
Lung Inflation ◽  
Fractional Concentration ◽  
Residual Capacity ◽  
Upward Direction ◽  
Breath Cycle

The effects of CO2 concentration on the timing of inspiratory duration (TI) and expiratory duration (TE) and the responses to lung inflation were studied in decerebrate paralyzed cats. With lung volume held at functional residual capacity during the breath cycle, hypercapnia (fractional concentration of inspired CO2 = 0.04) caused variable changes in TI and significant increases in TE. To obtain the Breuer-Hering threshold relationship [tidal volume (VT) vs. TI] and the timing relationship between TE and the preceding TI (TE vs. TI), ramp inflations of various sizes were used to terminate inspiration at different times in the breath cycle. Hypercapnia caused the VT vs. TI curves to shift in an upward direction so that at higher lung volumes TI was lengthened. Also, the slope of the TE vs. TI relationship was increased. The results suggest that hypercapnia diminished the sensitivity of the Breuer-Hering reflex to the lung volume, thus allowing volume to increase with little effect on TI. In addition, TE appears to become more sensitive to changes in the preceding TI. A model is presented which provides a possible neural mechanism for these responses.

Hering-Breuer reflex and respiratory system compliance in the first year of life: a longitudinal study

1994 ◽  
Vol 76 (2) ◽  
pp. 650-656 ◽  
Author(s):  
P. S. Rabbette ◽  
M. E. Fletcher ◽  
C. A. Dezateux ◽  
H. Soriano-Brucher ◽  
J. Stocks
Keyword(s):  
Respiratory System ◽  
Relative Strength ◽  
Reflex Response ◽  
Respiratory System Compliance ◽  
Lung Inflation ◽  
Airway Occlusion ◽  
Age Related ◽  
Healthy Infants ◽  
Occlusion Technique ◽  
Relative Change

The airway occlusion technique for measuring passive respiratory mechanics in infants relies on an ability to evoke the Hering-Breuer lung inflation reflex (HBR). However, there is conflicting evidence regarding the persistence of the HBR beyond the early newborn period. This study was designed to assess maturational changes in HBR activity and passive total respiratory system compliance (Crs) in healthy infants during the 1st yr of life. The strength of the HBR was assessed from the relative change in expiratory time (TE) after brief end-inspiratory airway occlusions compared with resting TE during spontaneous breathing. Crs was measured using the multiple-occlusion technique. Paired measurements of HBR activity and Crs were obtained during sedated sleep in 30 infants at 4–8 wk and at 1 yr of age. Significant HBR activity during tidal breathing persisted throughout the 1st yr of life, with TE increasing during occlusion by at least 26% in every infant. However, the relative strength of the reflex response decreased from a mean of 88.3% (range, 34–160%) at approximately 6 wk to 50.3% (range, 26–125%) by 1 yr of age (P < 0.001). All infants showed an increase in Crs with age, with mean Crs increasing from 60.1 +/- 8.9 (SD) to 149.0 +/- 20.6 ml/kPa between 6 wk and 1 yr. However, there was no apparent relationship between the magnitude of decline in HBR response and the age-related changes in Crs.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of five human anesthetics on respiratory control in cats

1978 ◽  
Vol 44 (4) ◽  
pp. 596-606 ◽  
Author(s):  
M. Younes ◽  
M. Youssef
Keyword(s):  
Chest Wall ◽  
Respiratory Control ◽  
Muscle Recruitment ◽  
Expiratory Muscle ◽  
Airway Occlusion ◽  
Vagal Cooling ◽  
Vagal Influence

The effect of halothane, fentanyl, Innovar, thiopental, and ketamine on inspiratory output, vagal influence, and chest wall reflex was assessed in seven cats lightly anesthetized with pentobarbital, using the method of airway occlusion with and without rapid vagal cooling. All anesthetics depressed inspiratory output, as expressed by deltaP/deltat, of the first occluded inspiration. However, only halothane depressed peak inspiratory output (Pmax). Phasic vagal influence was markedly depressed by 2% halothane but was preserved under other anesthetics. The ability to induce tonic vagal influence (expiratory muscle recruitment) was lost under halothane. Inspiratory inhibitory chest wall reflex was evident in two cats during airway occlusion. Addition of any test anesthetic abolished the reflex. It is concluded that halothane should be avoided in studies dealing with assessment of vagal influence.

Effects of tracheal airway occlusion on hyoid muscle length and upper airway volume

1989 ◽  
Vol 67 (6) ◽  
pp. 2296-2302 ◽  
Author(s):  
E. van Lunteren ◽  
M. A. Haxhiu ◽  
N. S. Cherniack
Keyword(s):  
Tidal Volume ◽  
Muscle Length ◽  
Upper Airway ◽  
Lung Inflation ◽  
Airway Occlusion ◽  
Muscle Shortening ◽  
Tidal Changes ◽  
Length Changes ◽  
Complex Relationships ◽  
Upper Airway Muscles

Complex relationships exist among electromyograms (EMGs) of the upper airway muscles, respective changes in muscle length, and upper airway volume. To test the effects of preventing lung inflation on these relationships, recordings were made of EMGs and length changes of the geniohyoid (GH) and sternohyoid (SH) muscles as well as of tidal changes in upper airway volume in eight anesthetized cats. During resting breathing, tracheal airway occlusion tended to increase the inspiratory lengthening of GH and SH. In response to progressive hypercapnia, the GH eventually shortened during inspiration in all animals; the extent of muscle shortening was minimally augmented by airway occlusion despite substantial increases in EMGs. SH lengthened during inspiration in six of eight animals under hypercapnic conditions, and in these cats lengthening was greater during airway occlusion even though EMGs increased. Despite the above effects on SH and GH length, upper airway tidal volume was increased significantly by tracheal occlusion under hypercapnic conditions. These data suggest that the thoracic and upper airway muscle reflex effects of preventing lung inflation during inspiration act antagonistically on hyoid muscle length, but, because of the mechanical arrangement of the hyoid muscles relative to the airway and thorax, they act agonistically to augment tidal changes in upper airway volume. The augmentation of upper airway tidal volume may occur in part as a result of the effects of thoracic movements being passively transmitted through the hyoid muscles.

Respiratory system compliance as seen from the cardiac fossa

1982 ◽  
Vol 53 (1) ◽  
pp. 57-62 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Left Ventricle ◽  
Chest Wall ◽  
Respiratory System ◽  
Shape Change ◽  
Left Ventricular ◽  
Respiratory System Compliance ◽  
Lung Volumes ◽  
Lung Inflation ◽  
Cardiac Filling ◽  
Different Levels

Changes in cardiac size and shape should impose stresses on the surrounding lung and chest wall. To examine pressure-volume relationships of the cardiac fossa we measured pressures required to increase the pericardial volume of freshly killed dogs at different levels of lung inflation, first by expanding the pericardium uniformly and then by expanding only the left ventricle. In both cases we obtained linear pressure-volume relationships, the slopes of which expressed an apparent compliance. Compliance decreased as lung volumes were increased by raising end-expiratory pressure, and compliance with symmetrical pericardial filling exceeded that with asymmetrical (left ventricular) distension. These compliances were compared with the total respiratory system compliance measured during tidal ventilation, and we found that the compliance of the cardiac fossa was significantly less than would be predicted from lung and chest wall compliances as classically measured. We concluded that the respiratory system imposes a finite compliance load on cardiac filling that raises local epicardial pressure above ambient pleural pressure. This respiratory system load depends upon lung volume and the cardiac shape change.

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