scholarly journals Dysfunction of the canine respiratory muscle pump in ascites

2007 ◽  
Vol 102 (2) ◽  
pp. 650-657 ◽  
Author(s):  
Dimitri Leduc ◽  
André De Troyer
Keyword(s):  
Minute Ventilation ◽  
Blood Gases ◽  
Neural Drive ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Arterial Blood ◽  
Airway Opening ◽  
Anesthetized Dogs ◽  
Inspiratory Activity

Ascites, a complicating feature of many diseases of the liver and peritoneum, commonly causes dyspnea. The mechanism of this symptom, however, is uncertain. In the present study, progressively increasing ascites was induced in anesthetized dogs, and the hypothesis was initially tested that ascites increases the impedance on the diaphragm and, so, adversely affects the lung-expanding action of the muscle. Ascites produced a gradual increase in abdominal elastance and an expansion of the lower rib cage. Concomitantly, the caudal displacement of the diaphragm and the fall in airway opening pressure during isolated stimulation of the phrenic nerves decreased markedly; transdiaphragmatic pressure during phrenic stimulation also decreased. To assess the adaptation to ascites of the respiratory system overall, we subsequently measured the changes in lung volume, the arterial blood gases, and the electromyogram of the parasternal intercostal muscles during spontaneous breathing. Tidal volume and minute ventilation decreased progressively as ascites increased, leading to an increase in arterial Pco2 and parasternal intercostal inspiratory activity. It is concluded that 1) ascites, acting through an increase in abdominal elastance and an expansion of the lower rib cage, impairs the lung-expanding action of the diaphragm; 2) this impairment elicits a compensatory increase in neural drive to the inspiratory muscles, but the compensation is not sufficient to maintain ventilation; and 3) dyspnea in this setting results in part from the dissociation between increased neural drive and decreased ventilation.

Respiratory response to abdominal and rib cage muscle paralysis in dogs

1993 ◽  
Vol 74 (5) ◽  
pp. 2309-2317 ◽  
Author(s):  
J. F. Brichant ◽  
M. Gorini ◽  
A. De Troyer
Keyword(s):  
Tidal Volume ◽  
Abdominal Cavity ◽  
Emg Activity ◽  
Abdominal Muscles ◽  
Respiratory Response ◽  
Muscle Paralysis ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Arterial Blood

To assess the respiratory response to abdominal and rib cage muscle paralysis, we measured tidal volume, esophageal and gastric pressures, arterial blood gases, and the electromyogram (EMG) of the diaphragm during progressive epidural anesthesia (lidocaine 2%) in 35 supine anesthetized dogs. The EMG activity of the diaphragm was measured with fine-wire electrodes; the abdominal cavity was thus left intact. Paralysis of the abdominal muscles alone did not produce any alterations. In contrast, when all rib cage muscles were also paralyzed, there were substantial increases in the peak height and the rate of rise of diaphragmatic EMG activity that were associated with a decrease in tidal volume and an increase in arterial PCO2 (PaCO2); swings in transdiaphragmatic pressure, however, were unchanged. The increased diaphragmatic activation due to rib cage muscle paralysis persisted after bilateral cervical vagotomy and was well explained by the increased PaCO2. These observations indicate that in the dog 1) the rib cage muscles contribute significantly to tidal volume, and their paralysis causes, through the increased hypercapnic drive, a compensatory increase in diaphragmatic activation; and 2) the rib cage inspiratory muscles enhance the diaphragm's ability to generate pressure during breathing.

Accessory muscle activity during sleep in chronic obstructive pulmonary disease

1984 ◽  
Vol 57 (4) ◽  
pp. 1011-1017 ◽  
Author(s):  
M. W. Johnson ◽  
J. E. Remmers
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Minute Ventilation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Inspiratory Activity ◽  
Increased Activity ◽  
Severe Copd

Hypoventilation contributes to oxyhemoglobin desaturation during rapid-eye-movement (REM) sleep in patients with severe chronic obstructive pulmonary disease (COPD). Due to hyperinflated lungs these patients have mechanically impaired diaphragms and increased activity of other inspiratory muscles while awake. We speculated that rib cage (RC) inspiratory muscles might lose activity during REM, thereby contributing to hypoventilation. We therefore recorded scalene (SCA) and sternocleidomastoid (SCM) electromyorgrams in six subjects with severe COPD. SCA activity decreased 76% (P less than 0.001), from non-REM (NREM) to tonic REM and decreased an additional 17% during phasic REM. SCM activity was much more variable during NREM but when present also decreased during REM. SCA activity correlated strongly with RC excursion. SCA and SCM activity, RC excursion, estimates of minute ventilation, and oxyhemoglobin saturation all decreased in parallel. Expiratory activity of the SCA and SCM, present during wakefulness and NREM, disappeared during REM. We conclude that loss of inspiratory activity of rib cage muscles during REM causes chest wall distortion and hypoventilation in patients with severe COPD. Loss of expiratory activity of these muscles may contribute to a decrease in end-expiratory volume and thereby to a deterioration of pulmonary gas exchange.

Pleural pressure increases during inspiration in the zone of apposition of diaphragm to rib cage

1988 ◽  
Vol 65 (5) ◽  
pp. 2207-2212 ◽  
Author(s):  
W. F. Urmey ◽  
A. De Troyer ◽  
K. B. Kelly ◽  
S. H. Loring
Keyword(s):  
Esophageal Pressure ◽  
Pleural Pressure ◽  
Abdominal Pressure ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Direct Measurements ◽  
Anesthetized Dogs ◽  
Theoretical Mechanism ◽  
Phrenic Stimulation ◽  
Anatomic Region

The zone of apposition of diaphragm to rib cage provides a theoretical mechanism that may, in part, contribute to rib cage expansion during inspiration. Increases in intra-abdominal pressure (Pab) that are generated by diaphragmatic contraction are indirectly applied to the inner rib cage wall in the zone of apposition. We explored this mechanism, with the expectation that pleural pressure in this zone (Pap) would increase during inspiration and that local transdiaphragmatic pressure in this zone (Pdiap) must be different from conventionally determined transdiaphragmatic pressure (Pdi) during inspiration. Direct measurements of Pap, as well as measurements of pleural pressure (Ppl) cephalad to the zone of apposition, were made during tidal inspiration, during phrenic stimulation, and during inspiratory efforts in anesthetized dogs. Pab and esophageal pressure (Pes) were measured simultaneously. By measuring Ppl's with cannulas placed through ribs, we found that Pap consistently increased during both maneuvers, whereas Ppl and Pes decreased. Whereas changes in Pdi of up to -19 cmH2O were measured, Pdiap never departed from zero by greater than -4.5 cmH2O. We conclude that there can be marked regional differences in Ppl and Pdi between the zone of apposition and regions cephalad to the zone. Our results support the concept of the zone of apposition as an anatomic region where Pab is transmitted to the interior surface of the lower rib cage.

Ventilatory responses of hamsters and rats to hypoxia and hypercapnia

1985 ◽  
Vol 59 (6) ◽  
pp. 1955-1960 ◽  
Author(s):  
B. R. Walker ◽  
E. M. Adams ◽  
N. F. Voelkel
Keyword(s):  
Duty Cycle ◽  
Minute Ventilation ◽  
Natural Habitat ◽  
Blood Gases ◽  
Atmospheric Conditions ◽  
Arterial Blood Gases ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Rat Experiments ◽  
Fossorial Species

As a fossorial species the hamster differs in its natural habitat from the rat. Experiments were performed to determine possible differences between the ventilatory responses of awake hamsters and rats to acute exposure to hypoxic and hypercapnic environments. Ventilation was measured with the barometric method while the animals were conscious and unrestrained in a sealed plethysmograph. Tidal volume (VT), respiratory frequency (f), and inspiratory (TI) and expiratory (TE) time measurements were made while the animals breathed normoxic (30% O2), hypercapnic (5% CO2), or hypoxic (10% O2) gases. Arterial blood gases were also measured in both species while exposed to each of these atmospheric conditions. During inhalation of normoxic gas, the VT/100 g was greater and f was lower in the hamster than in the rat. Overall minute ventilation (VE/100 g) in the hamster was less than in the rat, which was reflected in the lower PO2 and higher PCO2 of the hamster arterial blood. When exposed to hypercapnia, the hamster increased VE/100 g solely through VT; however, the VE/100 g increase was significantly less than in the rat. In response to hypoxia, the hamster and rat increased VE/100 g by similar amounts; however, the hamster VE/100 g increase was through f alone, whereas the rat increased both VT/100 g and f. Mean airflow rates (VT/TI) were no different in the hamster or rat in each gas environment; therefore most of the ventilatory responses were the result of changes in TI and TE and respiratory duty cycle (TI/TT).

Effect of pulmonary arterial PCO2 on breathing pattern

1988 ◽  
Vol 64 (5) ◽  
pp. 1844-1850 ◽  
Author(s):  
E. R. Schertel ◽  
D. A. Schneider ◽  
L. Adams ◽  
J. F. Green
Keyword(s):  
Breathing Pattern ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Middle Level ◽  
Positive Pressure ◽  
Breathing Patterns ◽  
Arterial Pco2 ◽  
Anesthetized Dogs ◽  
Steady State Levels ◽  
Pulmonary Arterial

We studied breathing patterns and tidal volume (VT)-inspiratory time (TI) relationships at three steady-state levels of pulmonary arterial PCO2 (PpCO2) in 10 anesthetized dogs. To accomplish this we isolated and then separately pump perfused the pulmonary and systemic circulations, which allowed us to control blood gases in each circuit independently. To ventilate the lungs at a rate and depth determined by central drive, we used an electronically controlled positive-pressure ventilator driven by inspiratory phrenic neural activity. Expiratory time (TE) varied inversely with PpCO2 over the range of PpCO2 from approximately 20 to 80 Torr. VT and TI increased with rising PpCO2 over the range from approximately 20 to 45 Torr but did not change further as PpCO2 was raised above the middle level of approximately 45 Torr. Thus minute ventilation increased as a function of TE and VT as PpCO2 was increased over the lower range and increased solely as a function of TE as PpCO2 was increased over the upper range. The VT-TI relationship shifted leftward on the time axis as PpCO2 was lowered below the middle level but did not shift in the opposite direction as PpCO2 was raised above the middle level. In addition to its effect on breathing pattern, we found that pulmonary hypocapnia depressed inspiratory drive.

scholarly journals Measuring the human ventilatory and cerebral blood flow response to CO2: a technical consideration for the end-tidal-to-arterial gas gradient

2016 ◽  
Vol 120 (2) ◽  
pp. 282-296 ◽  
Author(s):  
Michael M. Tymko ◽  
Ryan L. Hoiland ◽  
Tomas Kuca ◽  
Lindsey M. Boulet ◽  
Joshua C. Tremblay ◽  
...  
Keyword(s):  
Blood Flow ◽  
Minute Ventilation ◽  
Linear Regression Analysis ◽  
Blood Gases ◽  
Prediction Equation ◽  
Flow Response ◽  
Arterial Blood ◽  
Reactivity Test ◽  
End Tidal ◽  
Gas Gradients

Our aim was to quantify the end-tidal-to-arterial gas gradients for O2 (PET-PaO2) and CO2 (Pa-PETCO2) during a CO2 reactivity test to determine their influence on the cerebrovascular (CVR) and ventilatory (HCVR) response in subjects with (PFO+, n = 8) and without (PFO−, n = 7) a patent foramen ovale (PFO). We hypothesized that 1) the Pa-PETCO2 would be greater in hypoxia compared with normoxia, 2) the Pa-PETCO2 would be similar, whereas the PET-PaO2 gradient would be greater in those with a PFO, 3) the HCVR and CVR would be underestimated when plotted against PETCO2 compared with PaCO2, and 4) previously derived prediction algorithms will accurately target PaCO2. PETCO2 was controlled by dynamic end-tidal forcing in steady-state steps of −8, −4, 0, +4, and +8 mmHg from baseline in normoxia and hypoxia. Minute ventilation (V̇E), internal carotid artery blood flow (Q̇ICA), middle cerebral artery blood velocity (MCAv), and temperature corrected end-tidal and arterial blood gases were measured throughout experimentation. HCVR and CVR were calculated using linear regression analysis by indexing V̇E and relative changes in Q̇ICA, and MCAv against PETCO2, predicted PaCO2, and measured PaCO2. The Pa-PETCO2 was similar between hypoxia and normoxia and PFO+ and PFO−. The PET-PaO2 was greater in PFO+ by 2.1 mmHg during normoxia ( P = 0.003). HCVR and CVR plotted against PETCO2 underestimated HCVR and CVR indexed against PaCO2 in normoxia and hypoxia. Our PaCO2 prediction equation modestly improved estimates of HCVR and CVR. In summary, care must be taken when indexing reactivity measures to PETCO2 compared with PaCO2.

Naloxone alters the early response to an inspiratory flow-resistive load

1989 ◽  
Vol 67 (5) ◽  
pp. 1747-1753 ◽  
Author(s):  
A. T. Scardella ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Tidal Volume ◽  
Blood Gases ◽  
Inspiratory Flow ◽  
Abdominal Muscles ◽  
Base Line ◽  
Resistive Load ◽  
Endogenous Opioid ◽  
Transdiaphragmatic Pressure ◽  
Arterial Blood ◽  
Gastric Pressure

In a previous study in unanesthetized goats, we demonstrated that cerebrospinal fluid levels of beta-endorphin were significantly elevated after 2.5 h of inspiratory flow-resistive loading. Naloxone (NLX) (0.1 mg/kg) administration partially and transiently reversed the tidal volume depression seen during loading. In the current study, we tested the hypothesis that endogenous opioid elaboration results in depression of respiratory output to the diaphragm. In six studies of five unanesthetized goats, tidal volume (VT), transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi), and arterial blood gases were monitored. A continuous NLX (0.1 mg/kg) or saline (SAL) infusion was begun 5 min before an inspiratory flow-resistive load of 120 cmH2O.l-1.s was imposed. Our data show that the depression of VT induced by the load was prevented by NLX as early as 15 min and persisted for 2 h. At 2 h, Pdi was still 294 +/- 45% of the base-line value compared with 217 +/- 35% during SAL. There was no difference in EMGdi between the groups at any time. However, the augmentation of Pdi was associated with a greater increase in end-expiratory gastric pressure in the NLX group. We conclude that the reduction in VT and Pdi associated with endogenous opioid elaboration is not mediated by a decrease in neural output to the diaphragm, but it appears to be the result of a decrease in respiratory output to the abdominal muscles.

Stimulation of ventilation in emphysema by passively induced body motion

1962 ◽  
Vol 17 (5) ◽  
pp. 771-774 ◽  
Author(s):  
Herman F. Froeb
Keyword(s):  
Carbon Dioxide ◽  
Technical Assistance ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Body Motion ◽  
Therapeutic Tool ◽  
Arterial Blood ◽  
Weak Muscle ◽  
Normal Males

The ventilatory stimulation arising from two different forms of passively induced body motion was chosen for study of 14 male emphysematous subjects with hypercapnia and impaired ventilatory response to carbon dioxide. Nine normal males served as controls. The object of the study was to determine whether the stimulus to ventilation from passive body motion was intact in diseased subjects and whether it could serve as a therapeutic tool by bringing about a reduction in blood carbon dioxide. The results revealed that the stimulus to ventilation was mild and comparable in both groups but was associated with two to three times more oxygen per extra liter of minute ventilation in the diseased subjects. There were no significant changes in the arterial blood gases. It was concluded that the stimulus to ventilation from passive body motion arises from weak muscle action and has no therapeutic application in emphysematous subjects as a means of lowering the PaCOCO2. Note: (With the Technical Assistance of Mabel Pearson, Roy Engstrom, Christa McReynolds, and Carol Kennedy) Submitted on March 5, 1962

Partitioning of inspiratory pressure swings between diaphragm and intercostal/accessory muscles

1978 ◽  
Vol 44 (2) ◽  
pp. 200-208 ◽  
Author(s):  
P. T. Macklem ◽  
D. Gross ◽  
G. A. Grassino ◽  
C. Roussos
Keyword(s):  
Total Pressure ◽  
Pleural Pressure ◽  
Inspiratory Pressure ◽  
Abdominal Pressure ◽  
Abdominal Muscles ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Accessory Muscle ◽  
Inspiratory Muscles ◽  
Accessory Muscles

We tested the hypothesis that the inspiratory pressure swings across the rib-cage pathway are the sum of transdiaphragmatic pressure (Pdi) and the pressures developed by the intercostal/accessory muscles (Pic). If correct, Pic can only contribute to lowering pleural pressure (Ppl), to the extent that it lowers abdominal pressure (Pab). To test this we measured Pab and Ppl during during Mueller maneuvers in which deltaPab = 0. Because there was no outward displacement of the rib cage, Pic must have contributed to deltaPpl, as did Pdi. Under these conditions the total pressure developed by the inspiratory muscles across the rib-cage pathway was less than Pdi + Pic. Therefore, we rejected the hypothesis. A plot of Pab vs. Ppl during relaxation allows partitioning of the diaphragmatic and intercostal/accessory muscle contributions to inspiratory pressure swings. The analysis indicates that the diaphragm can act both as a fixator, preventing transmission of Ppl to the abdomen and as an agonist. When abdominal muscles remain relaxed it only assumes the latter role to the extent that Pab increases.

Response of newborn lambs to CO-induced hypoxia

1988 ◽  
Vol 64 (5) ◽  
pp. 1870-1877 ◽  
Author(s):  
M. A. Bureau ◽  
J. L. Carroll ◽  
E. Canet
Keyword(s):  
Minute Ventilation ◽  
Blood Gases ◽  
Periodic Breathing ◽  
Respiratory Frequency ◽  
Gas Mixture ◽  
Arterial Blood Gases ◽  
Small Shift ◽  
Arterial Blood ◽  
The Right ◽  
Very High

This study was undertaken to measure the neonate's response to CO-induced hypoxia in the first 10 days of life. CO breathing was used to induce hypoxia because CO causes tissue hypoxia with no or minimal chemoreceptor stimulation. An inspired gas mixture of 0.25 to 0.5% CO in air was used to raise the blood carboxyhemoglobin (HbCO) progressively from 0 to 60% over approximately 20 min. The study, conducted in awake conscious lambs aged 2 and 10 days, consisted in measuring the response of ventilation and the change in arterial blood gases during the rise of HbCO. The results showed that the 2- and 10-day-old lambs tolerated very high HbCO levels without an increase in minute ventilation (VE) and without metabolic acidosis. At both ages, HbCO caused no VE change until HbCO levels rose to between 45 and 50% after which the VE change was exponential in some animals but minimal in others. The VE change was brought about by a rise in tidal volume and respiratory frequency. During the period of maturation from 2 to 10 days, there was a small shift to the right in the VE-HbCO response. In the 10-day-old lambs the VE response to high HbCO was greater than that of the 2-day-olds because of the lambs' higher respiratory frequency response. Six of the 10-day-old lambs but only two of the 2-day-old lambs showed a hypoxic tachypnea to HbCO of 55–65%. None of the lambs developed periodic breathing, dysrhythmic breathing, or recurrent apneas with an HbCO level as high as 60%.(ABSTRACT TRUNCATED AT 250 WORDS)

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