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.

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.

Time and volume dependence of dead space in healthy and surfactant-depleted rat lungs during spontaneous breathing and mechanical ventilation

2013 ◽  
Vol 115 (9) ◽  
pp. 1268-1274 ◽  
Author(s):  
Constanze Dassow ◽  
David Schwenninger ◽  
Hanna Runck ◽  
Josef Guttmann
Keyword(s):  
Mechanical Ventilation ◽  
Tidal Volume ◽  
Dead Space ◽  
Spontaneous Breathing ◽  
Small Animals ◽  
Single Breath ◽  
Dead Space Volume ◽  
The Dead ◽  
Gas Volume ◽  
Space Volume

Volumetric capnography is a standard method to determine pulmonary dead space. Hereby, measured carbon dioxide (CO2) in exhaled gas volume is analyzed using the single-breath diagram for CO2. Unfortunately, most existing CO2 sensors do not work with the low tidal volumes found in small animals. Therefore, in this study, we developed a new mainstream capnograph designed for the utilization in small animals like rats. The sensor was used for determination of dead space volume in healthy and surfactant-depleted rats ( n = 62) during spontaneous breathing (SB) and mechanical ventilation (MV) at three different tidal volumes: 5, 8, and 11 ml/kg. Absolute dead space and wasted ventilation (dead space volume in relation to tidal volume) were determined over a period of 1 h. Dead space increase and reversibility of the increase was investigated during MV with different tidal volumes and during SB. During SB, the dead space volume was 0.21 ± 0.14 ml and increased significantly at MV to 0.39 ± 0.03 ml at a tidal volume of 5 ml/kg and to 0.6 ± 0.08 ml at a tidal volume of 8 and 11 ml/kg. Dead space and wasted ventilation during MV increased with tidal volume. This increase was mostly reversible by switching back to SB. Surfactant depletion had no further influence on the dead space increase during MV, but impaired the reversibility of the dead space increase.

Pressure-controlled mechanical ventilation

2016 ◽  
Author(s):  
Thomas Muders ◽  
Christian Putensen
Keyword(s):  
Mechanical Ventilation ◽  
Tidal Volume ◽  
Spontaneous Breathing ◽  
Airway Pressure ◽  
Gas Flow ◽  
Conventional Mechanical Ventilation ◽  
Lung Inflation ◽  
Cycle Times ◽  
Airway Pressures ◽  
Pressure Controlled

Beside reduction in tidal volume limiting peak airway pressure minimizes the risk for ventilator-associated-lung-injury in patients with acute respiratory distress syndrome. Pressure-controlled, time-cycled ventilation (PCV) enables the physician to keep airway pressures under strict limits by presetting inspiratory and expiratory pressures, and cycle times. PCV results in a square-waved airway pressure and a decelerating inspiratory gas flow holding the alveoli inflated for the preset time. Preset pressures and cycle times, and respiratory system mechanics affect alveolar and intrinsic positive end-expiratory (PEEPi) pressures, tidal volume, total minute, and alveolar ventilation. When compared with flow-controlled, time-cycled (‘volume-controlled’) ventilation, PCV results in reduced peak airway pressures, but higher mean airway. Homogeneity of regional peak alveolar pressure distribution within the lung is improved. However, no consistent data exist, showing PCV to improve patient outcome. During inverse ratio ventilation (IRV) elongation of inspiratory time increases mean airway pressure and enables full lung inflation, whereas shortening expiratory time causes incomplete lung emptying and increased PEEPi. Both mechanisms increase mean alveolar and transpulmonary pressures, and may thereby improve lung recruitment and gas exchange. However, when compared with conventional mechanical ventilation using an increased external PEEP to reach the same magnitude of total PEEP as that produced intrinsically by IRV, IRV has no advantage. Airway pressure release ventilation (APRV) provides a PCV-like squared pressure pattern by time-cycled switches between two continuous positive airway pressure levels, while allowing unrestricted spontaneous breathing in any ventilatory phase. Maintaining spontaneous breathing with APRV is associated with recruitment and improved ventilation of dependent lung areas, improved ventilation-perfusion matching, cardiac output, oxygenation, and oxygen delivery, whereas need for sedation, vasopressors, and inotropic agents and duration of ventilator support decreases.

Ventilatory and diaphragmatic EMG changes during negative-pressure ventilation in healthy subjects

1988 ◽  
Vol 64 (6) ◽  
pp. 2272-2278 ◽  
Author(s):  
D. O. Rodenstein ◽  
G. Cuttitta ◽  
D. C. Stanescu
Keyword(s):  
High Pressure ◽  
Tidal Volume ◽  
Negative Pressure ◽  
Healthy Subjects ◽  
Normal Subjects ◽  
Cortical Activity ◽  
Assisted Ventilation ◽  
Phase Lock ◽  
Negative Pressure Ventilation ◽  
Low Pressures

To evaluate the response of normal subjects to assisted ventilation, we studied 6 naive healthy subjects before and during negative-pressure ventilation (NPV) with "low" (-10 cmH2O) and "high" (-30 cmH2O) pressures in an Emerson tank respirator. Ventilation was measured with an inductive plethysmograph (Respitrace), and diaphragmatic electromyogram (DEMG) was studied with a bipolar esophageal electrode. During NPV a 1:1 phase lock was observed between subjects and iron lung frequency in all subjects. Tidal volume increased in most subjects, more with high than with low pressures (P less than 0.05), whereas DEMG increased, decreased, or showed no change. Postinspiratory inspiratory diaphragmatic activity (PIIA) significantly increased during high-pressure NPV and was accompanied by an increase in tonic DEMG in one-half of the subjects. Voluntary relaxation resulted in a decrease in DEMG and PIIA. We suggest that cortical activity can explain persistency of active breathing during negative-pressure ventilation.

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.

Sustained Improvement in Gas Exchange After Negative Pressure Ventilation for 8 Hours Per Day on 2 Successive Days in Chronic Airflow Limitation

1991 ◽  
Vol 144 (2) ◽  
pp. 390-394 ◽  
Author(s):  
Enrique Fernandez ◽  
Paltiel Weiner ◽  
Ephraim Meltzer ◽  
Mary M. Lutz ◽  
David B. Badish ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Negative Pressure ◽  
Airflow Limitation ◽  
Sustained Improvement ◽  
Negative Pressure Ventilation

Negative pressure ventilation decreases inflammation and lung edema during normothermic ex-vivo lung perfusion

2018 ◽  
Vol 37 (4) ◽  
pp. 520-530 ◽  
Author(s):  
Nader S. Aboelnazar ◽  
Sayed Himmat ◽  
Sanaz Hatami ◽  
Christopher W. White ◽  
Mohamad S. Burhani ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Ex Vivo ◽  
Lung Perfusion ◽  
Lung Edema ◽  
Ex Vivo Lung Perfusion ◽  
Negative Pressure Ventilation

Respiratory phase locking during mechanical ventilation in anesthetized human subjects

1986 ◽  
Vol 250 (5) ◽  
pp. R902-R909 ◽  
Author(s):  
C. Graves ◽  
L. Glass ◽  
D. Laporta ◽  
R. Meloche ◽  
A. Grassino
Keyword(s):  
Spontaneous Breathing ◽  
Breathing Pattern ◽  
Human Subjects ◽  
Phase Locking ◽  
Phase Relationship ◽  
Mechanical Ventilator ◽  
Lung Inflation ◽  
Fixed Phase ◽  
Simple Phase ◽  
Ventilator Settings

The coupling patterns between the rhythm of a mechanical ventilator and the rhythm of spontaneous breathing were studied in enflurane-anesthetized adult human subjects. The spontaneous breathing pattern was altered in response to different frequencies and amplitudes of forced lung inflations. A 1:1 phase locking (the frequency of the mechanical ventilator is matched by the frequency of spontaneous breathing with a fixed phase between the 2 rhythms) was observed in a range of up to +/- 40% of some of the subject's spontaneous breathing frequencies. During 1:1 phase locking, there were marked changes in the expiratory duration as measured from the electromyogram of the diaphragm. The phase relationship between onset of inflation and onset of inspiration depended on the frequency and amplitude of mechanical inflation. At ventilator settings that did not give 1:1 phase locking, other simple phase-locked patterns, such as 1:2 and 2:1, or irregular non-phase-locked patterns were observed. Reflexes arising from lung inflation, which may underlie the entrainment, are discussed in the context of these results.

Changing effect of lung volume on respiratory drive in man

1975 ◽  
Vol 38 (5) ◽  
pp. 768-773 ◽  
Author(s):  
N. N. Stanley ◽  
M. D. Altose ◽  
S. G. Kelsen ◽  
C. F. Ward ◽  
N. S. Cherniack
Keyword(s):  
Human Subjects ◽  
Inhibitory Effect ◽  
Breath Holding ◽  
Breath Hold ◽  
Respiratory Drive ◽  
Lung Inflation ◽  
Single Breath ◽  
Single Breath Hold ◽  
Sustained Effect ◽  
Residual Capacity

Experiments were conducted on human subjects to study the effect of lung inflation during breath holding on respiratory drive. Two series of experiments were performed: the first to examine respiratory drive during a single breath hold, the second designed to examine the sustained effect of lung inflation on subsequent breath holds. The experiments involved breath holding begun either at the end of a normal expiration or after a maximum inspiration. When breath holding was repeated at 10-min intervals, the increase in BHT produced by lung inflation was greater in short breath holds (after CO2 rebreathing) than in long breath holds (after hyperventilation). If breath holds were made in rapid succession, the first breath hold was much longer when made at total lung capacity than at functional residual capacity, but this effect of lung inflation diminished in subsequent breath holds. It is concluded that the inhibitory effect of lung inflation decays during breath holding and is regained remarkably slowly during the period of breathing immediately after breath holding.

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