Effects of acute exposure to high altitude on ventilatory drive and respiratory pattern

1984 ◽  
Vol 56 (4) ◽  
pp. 1027-1031 ◽  
Author(s):  
N. K. Burki
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Progressive Increase ◽  
Acute Exposure ◽  
Respiratory Pattern ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Ventilatory Pattern ◽  
Ventilatory Drive ◽  
Mouth Occlusion Pressure

To assess changes in ventilatory regulation in terms of central drive and timing, on exposure to high altitude, and the effects of induced hyperoxia at high altitude, six healthy normal lowland subjects (mean age 19.5 +/- 1.64 yr) were studied at low altitude (518 m) and on the first 4 days at high altitude (3,940 m). The progressive increase in resting expired minute ventilation (VE; control mean 9.94 +/- 1.78 to 14.25 +/- 2.67 l/min on day 3, P less than 0.005) on exposure to high altitude was primarily due to a significant increase in respiratory frequency (f; control mean 15.6 +/- 3.5 breaths/min to 23.8 +/- 6.2 breaths/min on day 3, P less than 0.01) with no significant change in tidal volume (VT). The increase in f was due to significant decreases in both inspiratory (TI) and expiratory (TE) time per breath; the ratio of TI to TE increased significantly (control mean 0.40 +/- 0.08 to 0.57 +/- 0.14, P less than 0.025). Mouth occlusion pressure did not change significantly, nor did the ratio of VE to mouth occlusion pressure. The acute induction of hyperoxia for 10 min at high altitude did not significantly alter VE or the ventilatory pattern. These results indicate that acute exposure to high altitude in normal lowlanders causes an increase in VE primarily by an alteration in central breath timing, with no change in respiratory drive. The acute relief of high altitude hypoxia for 10 min has no effect on the increased VE or ventilatory pattern.

Augmentation of CO2 drives by chlormadinone acetate, a synthetic progesterone

1984 ◽  
Vol 56 (6) ◽  
pp. 1627-1632 ◽  
Author(s):  
H. Kimura ◽  
F. Hayashi ◽  
A. Yoshida ◽  
S. Watanabe ◽  
I. Hashizume ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Pressure Response ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Physiological Basis ◽  
Load Compensation ◽  
Chlormadinone Acetate ◽  
Arterial Blood ◽  
Resistive Loading

We studied 10 male subjects who were administered chlormadinone acetate (CMA), a potent synthetic progesterone, to clarify the physiological basis of its respiratory effects. Arterial blood gas tension, resting ventilation, and respiratory drive assessed by ventilatory and occlusion pressure response to CO2 with and without inspiratory flow-resistive loading were measured before and 4 wk after CMA administration. In all subjects, arterial PCO2 decreased significantly by 5.7 +/- 0.6 (SE) Torr with an increase in minute ventilation by 1.8 +/- 0.6 l X min-1, whereas no significant changes were seen in O2 uptake. During unloaded conditions, both slopes of occlusion pressure and ventilatory response to CO2 increased, being statistically significant in the former but showing nonsignificant trends in the latter. Furthermore, inspiratory flow-resistive loading (16 cmH2O X l(-1) X s) increased both slopes more markedly after CMA. The magnitudes of load compensation, assessed by the ratio of loaded to unloaded slope of the occlusion pressure response curve, were increased significantly. We concluded CMA is a potent respiratory stimulant that increases the CO2 chemosensitivity and neuromechanical drives in the load-compensation mechanism.

Effect of chest wall distortion on occlusion pressure and the preterm diaphragm

1983 ◽  
Vol 55 (2) ◽  
pp. 359-364 ◽  
Author(s):  
P. N. LeSouef ◽  
J. M. Lopes ◽  
S. J. England ◽  
M. H. Bryan ◽  
A. C. Bryan
Keyword(s):  
Chest Wall ◽  
Preterm Infants ◽  
Face Mask ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Transdiaphragmatic Pressure ◽  
Airway Occlusion ◽  
Mouth Pressure ◽  
Gastric Pressure ◽  
Mouth Occlusion Pressure

We studied the effect of chest wall distortion (CWD) on transdiaphragmatic pressure (Pdi) and/or mouth pressure during end-expiratory airway occlusions in seven preterm infants. We measured mouth occlusion pressure (Pmo) with a face mask and pressure transducer, gastric pressure (Pga) with a fluid-filled catheter, diaphragmatic electromyogram (Edi) using surface electrodes, and rib cage and abdominal motion using magnetometers. We reasoned that Pdi = Pmo - Pga on airway occlusion. Periods with maximal and periods with minimal CWD were compared. We found that 1) when CWD was minimal, an increase in Edi produced an increase in Pmo and Pdi in all infants; when CWD was greatest, large increases in Edi produced no increase in Pmo or Pdi in four infants; 2) when breaths with the same Pmo or Pdi from each period in each infant were compared, those from the period with greatest CWD had an increased Edi (mean increase 76%, P less than 0.005, and 144%, P less than 0.01, for Pmo and Pdi, respectively). We conclude that in preterm infants, Pmo can be a poor indicator of respiratory drive, and CWD markedly limits the effectiveness of the diaphragm as a force generator.

Relationship between inspiratory drive and perceived inspiratory effort in normal man

1990 ◽  
Vol 78 (5) ◽  
pp. 493-496 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. A. Calverley
Keyword(s):  
Ventilatory Response ◽  
Free Breathing ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Resistive Loading ◽  
Mouth Occlusion Pressure ◽  
The Individual ◽  
Induced Changes

1. To examine the relationship between the inspiratory effort sensation (IES) and respiratory drive as reflected by mouth occlusion pressure (P0.1) we have studied loaded and unloaded ventilatory responses to CO2 in 12 normal subjects. 2. The individual coefficient of variation of the effort sensation response to CO2 (IES/Pco2) between replicate studies was 21% and was similar to the variability of the ventilatory response (VE/Pco2) (18%) and the occlusion pressure response (P0.1/Pco2) (22%). 3. IES was well correlated with P0.1 (r >0.9) for both free-breathing and loaded runs. 4. Resistive loading reduced the ventilatory response to hypercapnia from 19.3 1 min−1 kPa−1 (sd 7.5) to 12.6 1 min−1 kPa−1 (sd 3.9) (P <0.01). IES and P0.1 responses increased with resistive loading from 2.28 (sd 0.9) to 3.15 (sd 1.1) units/kPa and 2.8 (sd 1.2) to 3.73 (sd 1.5) cmH2O/kPa, respectively (P <0.01). 5. Experimentally induced changes in Pco2 and respiratory impedance were accompanied by increases in IES and P0.1. We found no evidence that CO2 increased IES independently of its effect on respiratory drive.

scholarly journals Control of breathing during sleep assessed by proportional assist ventilation

1998 ◽  
Vol 84 (1) ◽  
pp. 3-12 ◽  
Author(s):  
S. Meza ◽  
E. Giannouli ◽  
M. Younes
Keyword(s):  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Control Of Breathing ◽  
Respiratory Drive ◽  
Proportional Assist Ventilation ◽  
End Tidal

Meza, S., E. Giannouli, and M. Younes. Control of breathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3–12, 1998.—We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (Vt) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in Vt because Pmus would be downregulated substantially as a result of small decreases in[Formula: see text]. In the presence of substantial nonchemical sources of drive [believed to be the case in rapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reduction in [Formula: see text] as the output related to the chemically insensitive drive source is amplified severalfold. Twelve normal subjects underwent polysomnography while connected to a PAV ventilator. Continuous positive air pressure (5.2 ± 2.0 cmH2O) was administered to stabilize the upper airway. PAV was increased in 2-min steps from 0 to 20, 40, 60, 80, and 90% of the subject’s elastance and resistance. Vt, respiratory rate, minute ventilation, and end-tidal CO2pressure were measured at the different levels, and Pmus was calculated. Observations were obtained in stage 2 sleep ( n = 12), slow-wave sleep ( n = 11), and REM sleep ( n = 7). In all cases, Pmus was substantially downregulated with increase in assist so that the increase in Vt, although significant ( P < 0.05), was small (0.08 liter at the highest assist). There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.

Response to external inspiratory resistive loading and bronchospasm in anesthetized dogs

1982 ◽  
Vol 53 (2) ◽  
pp. 355-360 ◽  
Author(s):  
J. Savoy ◽  
M. E. Arnup ◽  
N. R. Anthonisen
Keyword(s):  
Breathing Pattern ◽  
External Loading ◽  
Vagal Activity ◽  
Occlusion Pressure ◽  
Ventilatory Drive ◽  
Resistive Loading ◽  
Lung Resistance ◽  
Anesthetized Dogs ◽  
Mouth Occlusion Pressure ◽  
Pentobarbital Sodium Anesthesia

Mouth occlusion pressure (P0.1) and breathing-pattern responses to external inspiratory resistive loading and methacholine chloride-induced bronchospasm were assessed in six dogs under pentobarbital sodium anesthesia. There was no change in P0.1 with external loading, but, in response to bronchospasm, we observed a P0.1 increase proportional to the change in lung resistance. These results indicate that, unlike external loading, the ventilatory-drive adaptation to bronchospasm does not require consciousness of the animal. The breathing-pattern response to bronchospasm consisted of tachypnea associated with decreased tidal volume (VT), decreased inspiratory duration (TI), and unchanged mean inspiratory flow (VT/TI). In response to resistive loading there was no tachypnea, VT decreased, TI was unchanged, and VT/TI decreased. We suggest that in response to resistive loading there was no modification of vagal activity, whereas in bronchospasm there was an increase of vagal activity, which was responsible for the changes in breathing pattern and, at least in part, for the changes in P0.1.

Central cardiorespiratory effects of glutamate in dogs

1986 ◽  
Vol 60 (6) ◽  
pp. 2056-2062 ◽  
Author(s):  
C. H. Chiang ◽  
P. Pappagianopoulos ◽  
B. Hoop ◽  
H. Kazemi
Keyword(s):  
Arterial Pressure ◽  
Minute Ventilation ◽  
Respiratory Drive ◽  
Gamma Aminobutyric Acid ◽  
Cardiorespiratory Function ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Capillary ◽  
Artificial Cerebrospinal Fluid ◽  
Ventilatory Drive ◽  
Anesthetized Dogs

Metabolism of certain amino acid neurotransmitters such as glutamate and gamma-aminobutyric acid (GABA) are closely linked in the brain to CO2 fixation and H+ metabolism. Additionally they may also affect central modulation of cardiorespiratory function. Therefore central cardiorespiratory effects of L-glutamate were determined in lightly anesthetized dogs using ventriculocisternal perfusion with artificial cerebrospinal fluid (CSF) (pH 7.25–7.28) containing 30 or 60 mM glutamate at a flow rate of 1.0 ml/min for 20 min followed by perfusion with artificial CSF alone. Tidal volume and minute ventilation increased with 60 mM glutamate, as did respiratory drive. These changes returned to normal with mock CSF perfusion. Glutamate (30 mM) had no significant effect on ventilation. At both concentrations, glutamate significantly increased mean femoral arterial pressure and mean pulmonary arterial pressure, which was accompanied by bradycardia. All these increases rapidly returned to normal with mock CSF perfusion. Cardiac output and pulmonary capillary wedge pressure did not change with glutamate perfusion. The results suggest that glutamate may have a significant central excitatory role in modulation of ventilatory drive as well as of hemodynamic functions.

Changes in upper airway resistance during progressive normocapnic hypoxia in normal men

1991 ◽  
Vol 70 (2) ◽  
pp. 548-553 ◽  
Author(s):  
F. Maltais ◽  
L. Dinh ◽  
Y. Cormier ◽  
F. Series
Keyword(s):  
Functional Residual Capacity ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Baseline Period ◽  
Respiratory Drive ◽  
Nasal Resistance ◽  
Bias Flow ◽  
Residual Capacity ◽  
Mouth Occlusion Pressure ◽  
Normal Men

The effects of normocapnic progressive hypoxia on nasal and pharyngeal resistances were evaluated in nine normal men. To calculate resistances, upper airway pressures were measured with two low-bias flow catheters; one was placed at the tip of the epiglottis and the other in the posterior nasopharynx, and we measured flow with a Fleish no. 3 pneumotachograph connected to a tightly fitting mask. Both resistances were obtained during a baseline period and during progressive normocapnic hypoxia achieved by a rebreathing method. We collected the breath-by-breath values of upper airway resistances, minute ventilation, O2 and CO2 fractions, arterial O2 saturation (SaO2), and changes in functional residual capacity (inductance vest). The central respiratory drive was evaluated by the mouth occlusion pressure 0.1 s after the onset of inspiration (P0.1), and breath-by-breath P0.1 values were estimated by intrapolation from the linear relationship between P0.1 and SaO2. In each subject both resistances decreased during the hypoxic test. The slope of the decrease in resistance with decreasing SaO2 (%baseline/%SaO2) was steeper for pharyngeal resistance than for nasal resistance [2.67 +/- 0.29 and 1.61 +/- 0.25 (SE), respectively; P less than 0.05]. The slope of the decrease in resistance with increasing P0.1 (%baseline/cmH2O) was -0.24 +/- 0.05 for nasal resistance and -0.39 +/- 0.07 for pharyngeal resistance (P less than 0.05). Functional residual capacity progressively increased during the test, but the decrease in resistance was greater than expected from an isolated increase in lung volume. We conclude that nasal and pharyngeal resistances decrease during progressive normocapnic hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory Drive in Nonsmokers and Smokers Assessed by Passive Tilt and Mouth Occlusion Pressure

CHEST Journal ◽  
1985 ◽  
Vol 87 (1) ◽  
pp. 6-10 ◽  
Author(s):  
T.S. Chadha ◽  
E. Lang ◽  
S. Birch ◽  
M. A Sackner
Keyword(s):  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Mouth Occlusion Pressure

Ventilatory Pattern and Drive after Acute Myocardial Infarction

1980 ◽  
Vol 59 (2) ◽  
pp. 115-121 ◽  
Author(s):  
H. Clarke ◽  
S. Dhingra ◽  
N. R. Anthonisen
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Occlusion Pressure ◽  
Breathing Cycle ◽  
Left Heart Failure ◽  
Ventilatory Drive

1. In 18 patients with acute myocardial infarction, we measured ventilation, frequency, inspiratory duration and the pressure at the mouth 0.1 s after the onset of inspiration against an occluded airway; mean inspiratory flow and the fraction of the breathing cycle devoted to inspiration were calculated. Measurements were made on 2–3 consecutive days soon after admission and repeated 4–10 days after admission. 2. Eight patients showed no clinical evidence of left heart failure at any time; in these patients no changes in breathing pattern, ventilation or occlusion pressure were observed. 3. Ten patients were in heart failure, as judged by the presence of râles and/or hypoxaemia on day 1 of the study, and all had recovered on the last day. When in failure these patients demonstrated increased minute ventilation, occlusion pressure was increased more than was mean inspiratory flow and their breathing pattern was altered. Tidal volume was similar to that in patients without failure and did not change with time, but frequency was initially high and fell as recovery from failure occurred. The duration of inspiration was decreased during failure, so mean inspiratory flow was increased. The fraction of the breathing cycle devoted to inspiration was constant and similar to that in patients without failure. 4. While in failure no patients were acidotic and not all patients were hypoxaemic; administration of oxygen did not influence results in two patients during failure. 5. These results indicate that clinically detectable pulmonary oedema is associated with increased ventilatory drive, which cannot be explained on the basis of hypoxaemia or hypercapnia. The observed changes in breathing pattern were probably due at least in part to vagal reflexes, and these may have contributed to the increase in drive.

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