Breathing pattern and CO2 response in newborn rats before and during anesthesia

1985 ◽  
Vol 58 (6) ◽  
pp. 1988-1996 ◽  
Author(s):  
M. Saetta ◽  
J. P. Mortola
Keyword(s):  
Respiratory System ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Newborn Rats ◽  
Inspiratory Time ◽  
Co2 Response ◽  
Expiratory Time ◽  
Ketamine Anesthesia ◽  
Sustained Increase ◽  
Large Reserve

We have studied the breathing pattern (minute ventilation VE, tidal volume VT, and respiratory rate f) in newborn rats before and during barbiturate (20–30 mg/kg ip) or ketamine anesthesia (40–80 mg/kg ip). Animals were intact and prone in a flow plethysmograph in thermoneutral conditions. Before anesthesia, CO2 breathing (5 min in 5% and 5 min in 10% CO2 in O2) resulted in a substantial increase in VE (169 and 208%, respectively), which was maintained throughout the entire CO2 breathing period. This indicates that, despite the extremely large VE per kilogram at rest, in these small animals there is still a large reserve for a sustained increase in VE. During barbiturate, the resting VE dropped to 45% of control, due to a reduction in VT (83%) and f (59%). This latter result was due to a prolongation of the expiratory time (214%) with no significant changes in inspiratory time. CO2 response was also much depressed, to approximately 63% of the control. The late portion of the expiratory flow-volume curves, the slope of which represents the expiratory time constant of the system, was similar before and during anesthesia in approximately 50% of the animals, whereas it increased during anesthesia in the remaining animals. Although compliance of the respiratory system was generally unaltered, the increased impedance during anesthesia probably reflected an increased resistance. Qualitatively similar results were obtained during ketamine anesthesia. Therefore, as observed in adult mammals, anesthesia in newborn rats has a marked depressant effect on resting breathing pattern and CO2 response, occasionally accompanied by an increase in the expiratory impedance of the respiratory system.

Separation of factors responsible for change in breathing pattern induced by instrumentation

1985 ◽  
Vol 59 (5) ◽  
pp. 1515-1520 ◽  
Author(s):  
W. Perez ◽  
M. J. Tobin
Keyword(s):  
Tidal Volume ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Sensory Receptors ◽  
Inspiratory Time ◽  
Expiratory Time ◽  
Oral Breathing ◽  
Oral Stimulation ◽  
Additional Stimulation ◽  
Stimulation Of

Employment of mouthpiece and noseclips (MP + NC) has repeatedly been shown to increase tidal volume (VT), but its effect on respiratory frequency (f) and its subsets is controversial. The mechanisms accounting for this alteration in breathing pattern are poorly understood and may include stimulation of oral or nasal sensory receptors or alteration in the route of breathing. In this study we demonstrated that use of a MP + NC, compared with nonobtrusive measurement with a calibrated respiratory inductive plethysmograph, alters the majority of the volume and time indexes of breathing pattern, with increases in minute ventilation (P less than 0.01), VT (P less than 0.001), inspiratory time (TI, P less than 0.05), expiratory time (TE, P less than 0.05), mean inspiratory flow (P less than 0.05), and mean expiratory flow (P less than 0.05) and a decrease in f(P less than 0.05). Separating the potential mechanisms we found that when the respiratory route was not altered, independent oral stimulation (using an occluded MP) or nasal stimulation (by applying paper clips to the alae nasi) did not change the breathing pattern. In contrast, obligatory oral breathing without additional stimulation of the oral or nasal sensory receptors caused increases in VT (P less than 0.05), TI (P less than 0.05), and TE (P less than 0.01) and a fall in f(P less than 0.05). Heating and humidifying the inspired air did not prevent the alteration in breathing pattern with a MP. Thus change in the respiratory route is the major determinant of the alteration in breathing pattern with a MP + NC.

Enkephalin-induced changes in ventilation and ventilatory pattern in adult dogs

1983 ◽  
Vol 55 (4) ◽  
pp. 1311-1320 ◽  
Author(s):  
G. G. Haddad ◽  
M. R. Gandhi ◽  
G. M. Hochwald ◽  
T. L. Lai
Keyword(s):  
Receptor Agonist ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Periodic Breathing ◽  
Base Line ◽  
Inspiratory Time ◽  
Ventilatory Pattern ◽  
Induced Changes ◽  
Prior Administration

We studied the changes in ventilation induced by intracisternal administration of enkephalins in four unanesthetized adult dogs. Instantaneous minute ventilation (VT/TT) decreased markedly after D-Ala-Met-enkephalinamide (DAME). Mean VT/TT decreased maximally by 20-50 min after DAME and lasted an additional 15-60 min; by 2 h, VT/TT had returned to base line. Four doses (5, 25, 60, and 125 micrograms/kg) of DAME were used, and the ventilatory response depended on the dose. Mean inspiratory time decreased but mean expiratory time and mean TT showed a marked prolongation. Periodic breathing (2-3 breaths separated by long apneic pauses) occurred in every study and the frequency of sighs increased considerably. All these ventilatory changes were reversed by low doses of naloxone or naltrexone; in addition, VT/TT increased well above base line after the administration of these antagonists. However, naloxone did not increase VT/TT when injected without prior administration of DAME. We conclude that 1) the decrease in VT/TT is due to a decrease in respiratory duty cycle; 2) periodic breathing and increased frequency of sighs constitute part of the changes in the ventilatory pattern induced by DAME; 3) a ventilatory withdrawal reaction may occur after a receptor-agonist interaction of short duration; and 4) although enkephalins can modulate ventilation and the breathing pattern in a major way, these data provide no evidence suggesting that this modulation is tonic.

Airway anesthesia effects on hypercapnic breathing pattern in humans

1983 ◽  
Vol 55 (2) ◽  
pp. 368-376 ◽  
Author(s):  
T. Y. Sullivan ◽  
P. L. Yu
Keyword(s):  
Airway Resistance ◽  
Vital Capacity ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inspiratory Time ◽  
Abrupt Increase ◽  
Thoracic Gas Volume ◽  
Before And After ◽  
Gas Volume

Minute ventilation (VE) and breathing pattern during an abrupt increase in fractional CO2 were compared in 10 normal subjects before and after airway anesthesia. Subjects breathed 7% CO2-93% O2 for 5 min before and after inhaling aerosolized lidocaine. As a result of airway anesthesia, VE and tidal volume (VT) were greater during hypercapnia, but there was no effect on inspiratory time (TI). Therefore, airway anesthesia produced an increase in mean inspiratory flow (VT/TI) during hypercapnia. The increase in VT/TI was compatible with an increase in neuromuscular output. There was no effect of airway anesthesia on the inspiratory timing ratio or the shape and position of the curve relating VT and TI. We also compared airway resistance (Raw), thoracic gas volume, forced vital capacity, forced expired volume at 1s, and maximum midexpiratory flow rate before and after airway anesthesia. A small (0.18 cmH2O X l-1 X s) decrease in Raw occurred after airway anesthesia that did not correlate with the effect of airway anesthesia on VT/TI. We conclude that airway receptors accessible to airway anesthesia play a role in hypercapnic VE.

Effect of Continuous Positive Airway Pressure on the Ventilatory Response to CO2 in Preterm Infants

PEDIATRICS ◽  
1983 ◽  
Vol 71 (4) ◽  
pp. 634-638
Author(s):  
Manuel Durand ◽  
Ellen McCann ◽  
June P. Brady
Keyword(s):  
Tidal Volume ◽  
Preterm Infants ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Co2 Response ◽  
Expiratory Time ◽  
Ventilatory Response To Co2

The effect of continuous positive airway pressure (CPAP) on the ventilatory response to CO2 in newborn infants is unknown. The CO2 response to 4% CO2 in air was studied in nine preterm infants without lung disease before and during administration of CPAP (4 to 5 cm H2O) delivered by face mask. Minute ventilation, tidal volume, respiratory frequency, and end-tidal Pco2 were measured, and the slope and intercept of the CO2 response were calculated. Respiratory pattern and changes in oxygenation were also analyzed by measuring inspiratory and expiratory time, mean inspiratory flow, mean expiratory flow, effective respiratory timing, endtidal Po2, and transcutaneous Po2. CPAP significantly decreased minute ventilation from 278.7 to 197.6 mL/mm/kg (P < .001). Tidal volume and respiratory frequency were also significantly decreased. The slope of the CO2 response during CPAP was not significantly different from the slope before CPAP (36 v 33 mL/min/kg/mm Hg, P > .1), but the intercept was shifted to the right (P < .001). The decrease in respiratory frequency was primarily due to a prolongation of expiratory time (P < .05). In addition, transcutaneous Po2 increased during administration of CPAP (P < .001). These findings indicate that: (1) CPAP significantly decreases ventilation in preterm infants without lung disease, affecting both tidal volume and respiratory frequency; (2) CPAP does not appreciably alter the ventilatory response to CO2; (3) the changes in respiratory frequency are primarily accounted for by a prolongation of expiratory time; (4) CPAP improves oxygenation.

Effects of acute and chronic cocaine on breathing and chemosensitivity in awake rats

1994 ◽  
Vol 266 (3) ◽  
pp. R696-R701 ◽  
Author(s):  
T. Trippenbach ◽  
G. Kelly
Keyword(s):  
Breathing Pattern ◽  
Minute Ventilation ◽  
Co2 Response ◽  
Group 4 ◽  
Chronic Cocaine ◽  
Group 3 ◽  
Group 5 ◽  
Group 2 ◽  
Awake Rats ◽  
Group 1

The barometric method was used to study effects of acute (AC) and chronic cocaine (CC) on breathing and chemosensitivity in awake rats. Effects of AC were evaluated 15 min after daily intraperitoneal injections, and effects of CC were measured at each week of the 4-wk treatment. Sham rats (group 1, n = 10) were injected with NaCl (0.2 ml). Cocaine HCl was given daily in groups 2 (20 mg/kg, n = 5) and 3 (40 mg/kg, n = 10). Effects of AC on the respiratory responses to 10% O2 in N2 and 5% CO2 in 21% O2 were studied 15 min after the first injection of cocaine. Effects of CC on chemosensitivity were studied at weekly intervals. NaCl had no effects on the breathing pattern or chemosensitivity. During normoxia, AC caused an increase in respiratory rate in group 2 and rapid and shallow respiration in group 3. The effects were similar from the first to the last injection at week 4. Haloperidol, a dopamine (DA) receptor blocker, abolished (group 4, n = 8) or prevented (group 5, n = 9) effects of AC. CC had no effects in all normoxic rats. During exposure to either low O2 or high CO2 the AC-induced polypnea was replaced by deep and slow respiration. CC had no effects on CO2 response in all rats. In contrast, 10% O2 response of tidal volume in group 2 and minute ventilation in group 3 were attenuated at weeks 3 and 4 compared with control.(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragm and lung afferents contribute to inspiratory load compensation in awake ponies

1994 ◽  
Vol 76 (3) ◽  
pp. 1330-1339 ◽  
Author(s):  
H. V. Forster ◽  
T. F. Lowry ◽  
L. G. Pan ◽  
B. K. Erickson ◽  
M. J. Korducki ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Treadmill Exercise ◽  
Minute Ventilation ◽  
Inspiratory Time ◽  
Arterial Pco2 ◽  
Load Compensation ◽  
Expiratory Time ◽  
Inspiratory Load

We determined the effect of pulmonary vagal (hilar nerve) denervation (HND) and diaphragm deafferentation (DD) on inspiratory load compensation. We studied awake intact (I; n = 10), DD (n = 5), HND (n = 4), and DD+HND (n = 7) ponies at rest and during mild (1.8 mph, 5% grade) and moderate (1.8 mph, 15% grade) treadmill exercise before, during, and after resistance of the inspiratory circuit was increased from approximately 1.5 to approximately 20 cmH2O.l–1.s. During the first loaded breath in I ponies at rest, inspiratory time (TI) increased, expiratory time decreased, and inspiratory drive increased. There were minimal changes after the first breath, and inspiratory minute ventilation (VI) and arterial PCO2 did not change (P > 0.10) from control values. On the first loaded breath during exercise, TI increased but inspiratory drive either did not change or decreased from control values. TI and drive increased after the first breath, but the increases were insufficient to maintain VI and arterial PCO2 at control levels. First-breath load compensation remained after DD, HND, and DD+HND, but after DD+HND tidal volume and VI were compensated 5–10% less (P < 0.05) than in I ponies. In all groups inspiratory drive, tidal volume, and VI were markedly augmented on the first breath after loading was terminated with a gradual return toward control. We conclude that diaphragm and pulmonary afferents contribute to but are not essential for inspiratory load compensation in awake ponies.

Development of the ventilatory response to hypoxia in Swiss CD-1 mice

2000 ◽  
Vol 88 (5) ◽  
pp. 1907-1914 ◽  
Author(s):  
Dean M. Robinson ◽  
Henry Kwok ◽  
Brandon M. Adams ◽  
Karen C. Peebles ◽  
Gregory D. Funk
Keyword(s):  
Tidal Volume ◽  
Body Mass ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Developmental Changes ◽  
Hypoxic Exposure ◽  
Hypoxic Ventilatory Response ◽  
Expiratory Time ◽  
Ventilatory Response To Hypoxia

We examined developmental changes in breathing pattern and the ventilatory response to hypoxia (7.4% O2) in unanesthetized Swiss CD-1 mice ranging in age from postnatal day 0 to 42(P0–P42) using head-out plethysmography. The breathing pattern of P0 mice was unstable. Apneas were frequent at P0 (occupying 29 ± 6% of total time) but rare by P3 (5 ± 2% of total time). Tidal volume increased in proportion to body mass (∼10–13 ml/kg), but increases in respiratory frequency (f) (55 ± 7, 130 ± 13, and 207 ± 20 cycles/min for P0, P3, and P42, respectively) were responsible for developmental increases in minute ventilation (690 ± 90, 1,530 ± 250, and 2,170 ± 430 ml ⋅ min− 1 ⋅ kg− 1for P0, P3, and P42, respectively). Between P0 and P3, increases in f were mediated by reductions in apnea and inspiratory and expiratory times; beyond P3, increases were due to reductions in expiratory time. Mice of all ages showed a biphasic hypoxic ventilatory response, which differed in two respects from the response typical of most mammals. First, the initial hyperpnea, which was greatest in mature animals, decreased developmentally from a maximum, relative to control, of 2.58 ± 0.29 in P0 mice to 1.32 ± 0.09 in P42mice. Second, whereas ventilation typically falls to or below control in most neonatal mammals, ventilation remained elevated relative to control throughout the hypoxic exposure in P0 (1.73 ± 0.31), P3 (1.64 ± 0.29), and P9 (1.34 ± 0.17) mice but not in P19 or P42 mice.

Breathing patterns during varied activities

1992 ◽  
Vol 73 (3) ◽  
pp. 887-893 ◽  
Author(s):  
D. Paek ◽  
F. D. McCool
Keyword(s):  
Breathing Pattern ◽  
Minute Ventilation ◽  
Physical Activities ◽  
Breathing Cycle ◽  
Breathing Patterns ◽  
Inspiratory Time ◽  
Activity Effect ◽  
Surface Displacements ◽  
Arm Ergometry ◽  
Task Dependency

The level of ventilation attained and breathing patterns adopted during activity have important implications for the distribution and deposition of particles that are inhaled. However, breathing patterns and levels of ventilation adopted during specific physical activities are unknown. We used a noninvasive means of measuring ventilation in subjects performing a variety of activities (bicycling, arm ergometry, lifting, and pulling) during unencumbered (no mouthpiece) breathing and while breathing through a mouthpiece. Minute ventilation (VE), tidal volume (VT), inspiratory time (TI), and total breathing cycle time (TT) were measured initially both spirometrically and from body surface displacements. When a mouthpiece was used, VE and breathing patterns were significantly altered during all activities such that VE, VT, and TT increased by 16, 34, and 20%, respectively. This mouthpiece effect was attenuated at the higher levels of VE. A task dependency of breathing pattern was also noted such that there was much greater variability of VT and TI for a given VE during the lifting activity compared with bicycling (coefficient of variation for VT of 0.39 +/- 0.09 vs. 0.20 +/- 0.07, P less than 0.01; and for TI of 0.38 +/- 0.08 vs. 0.21 +/- 0.08, P less than 0.01). We conclude that a mouthpiece significantly alters breathing pattern during varied types and intensities of activities, and breathing patterns may differ significantly from one activity to another. When the total dose of particulates inhaled in the lung are assessed, the mouthpiece effect and activity effect on breathing pattern must be considered.

Preterm infants: ventilation and P100 changes with CO2 and inspiratory resistive loading

1985 ◽  
Vol 58 (6) ◽  
pp. 1982-1987 ◽  
Author(s):  
S. Duara ◽  
S. Abbasi ◽  
T. H. Shaffer ◽  
W. W. Fox
Keyword(s):  
Minute Ventilation ◽  
Resistive Load ◽  
Inspiratory Time ◽  
Co2 Response ◽  
Airway Occlusion ◽  
Time Ratio ◽  
Mouth Pressure ◽  
Resistive Loading ◽  
Ventilatory Effects ◽  
The Right

The ventilatory effects of inspiratory flow-resistive loading and increased chemical drive were measured in ten neonates during progressive hypercapnia in control and loaded states. Hypercapnia (mean increase PCO2 = 15–20) resulted from inspiring 8% CO2 in room air and inspiratory loading by a flow-resistive load = 100 cmH2O X l-1) X s. Hypercapnia produced an increase in group minute ventilation secondary to increasing tidal volumes and breathing frequencies. Loading shifted the minute ventilation-CO2 response to the right, and slopes decreased significantly (P less than 0.05) consequent to a significant decrease in the frequency-CO2 slopes (P less than 0.05), which became negative in four of the ten subjects. Mouth pressure measured at 100 ms after onset of inspiratory effort (P100) occlusion pressure-CO2 slopes measured in five subjects showed no significant increase with load application. Resistive loading produced significant increases in inspiratory time (P less than 0.02) and the inspiratory time/total breath time ratio (P less than 0.01). Airway occlusion elicited the Hering-Breuer reflex, with a significant increase in inspiratory time-to-total breath time ratio (P less than 0.01). The results show that the inspiratory resistive load produced ventilatory compromise in newborns and insufficient compensatory augmentation of central drive.

Effects of upper or lower airway anesthesia on hypercapnic ventilation in humans

1985 ◽  
Vol 59 (4) ◽  
pp. 1090-1097 ◽  
Author(s):  
P. A. Easton ◽  
C. Jadue ◽  
M. E. Arnup ◽  
R. C. Meatherall ◽  
N. R. Anthonisen
Keyword(s):  
Tidal Volume ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Lower Airway ◽  
Saline Control ◽  
Inspiratory Time ◽  
Lidocaine Solution ◽  
Normal Humans ◽  
Receptor Block ◽  
Ventilatory Response To Co2

To evaluate the contribution of vagal airway receptors to ventilatory control during hypercapnia, we studied 11 normal humans. Airway receptor block was induced by inhaling an aerosol of lidocaine; a preferential upper oropharyngeal block was also induced in a subgroup by gargling a solution of the anesthetic. Inhalation of lidocaine aerosol adequate to increase cough threshold, as measured by citric acid, did not change the ventilatory response to CO2, ratio of the change in minute ventilation to change in alveolar PCO2 (delta VI/delta PACO2), compared with saline control. Breathing pattern at mean CO2-stimulated ventilation of 25 l/min showed significantly decreased respiratory frequency, increased tidal volume, and prolonged inspiratory time compared with saline. Resting breathing pattern also showed significantly increased tidal volume and inspiratory time. In nine of the same subjects gargling a lidocaine solution adequate to extinguish gag response without altering cough threshold did not change delta VI/delta PACO2 or ventilatory pattern during CO2-stimulated or resting ventilation compared with saline. These results suggest that lower but not upper oropharyngeal vagal airway receptors modulate breathing pattern during hypercapnic as well as resting ventilation but do not affect delta VI/delta PACO2.

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