Hypoxic and hypercapnic ventilatory responses in Prader-Willi syndrome

1994 ◽  
Vol 77 (5) ◽  
pp. 2224-2230 ◽  
Author(s):  
R. Arens ◽  
D. Gozal ◽  
K. J. Omlin ◽  
F. R. Livingston ◽  
J. Liu ◽  
...  
Keyword(s):  
Sleep Disordered Breathing ◽  
Control Group ◽  
Prader Willi Syndrome ◽  
Ventilatory Control ◽  
Peripheral Chemoreceptor ◽  
Ventilatory Responses ◽  
Obese Control ◽  
The Mean ◽  
End Tidal ◽  
Arterial O2 Saturation

Abnormalities of ventilatory control may play a significant role in the pathophysiology of sleep-disordered breathing in patients with the Prader-Willi syndrome (PWS). We measured rebreathing hypercapnic and hypoxic ventilatory responses (HCVR and HPVR, respectively) during wakefulness in 8 nonobese PWS (NOB-PWS) and 9 obese PWS (OB-PWS) patients and compared their results with those from 24 healthy nonobese control (NOB-CON) and 10 obese control (OB-CON) subjects. The slope of HCVR was similar in NOB-PWS patients and NOB-CON subjects (NS). However, HCVR was significantly lower in OB-PWS patients than in OB-CON subjects (P < 0.02). In PWS patients, the mean point of origin of the positive slope of HCVR occurred at a significantly higher end-tidal PCO2 than in either control group. During isocapnic hypoxic challenges, six PWS patients had no significant HPVR. In the remainder, mean slopes of HPVR were -0.80 +/- 0.06 l.min-1.%arterial O2 saturation-1 in five NOB-PWS patients and -0.68 +/- 0.15 l.min-1.%arterial O2 saturation-1 in six OB-PWS patients. These responses were significantly decreased compared with those in the control groups (P < 0.006). We conclude that NOB-PWS patients have normal HCVR, which is blunted in OB-PWS patients. Furthermore, isocapnic HPVR is either absent or markedly reduced in PWS patients. The severity of abnormality of the HPVR is independent of the degree of obesity. We postulate that the primary abnormality of ventilatory control in PWS affects peripheral chemoreceptor pathways.

Developmental pattern of hypercapnic and hypoxic ventilatory responses from childhood to adulthood

1994 ◽  
Vol 76 (1) ◽  
pp. 314-320 ◽  
Author(s):  
C. L. Marcus ◽  
W. B. Glomb ◽  
D. J. Basinski ◽  
S. L. Davidson ◽  
T. G. Keens
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Body Size ◽  
Respiratory Rate ◽  
Body Surface ◽  
Vital Capacity ◽  
Developmental Pattern ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

The developmental pattern of ventilatory responses, through childhood and puberty into adulthood, is not known. Therefore we studied hypercapnic (HCVR) and hypoxic ventilatory responses (HOVR) in 59 subjects (29 males and 30 females) 4–49 yr of age, of whom 35 were children ( < 18 yr old). There was a significant correlation between HCVR and weight (r = 0.33, P < 0.02), vital capacity (r = 0.30, P < 0.05), and body surface area (r = 0.30, P < 0.05) but not height (r = 0.22, NS). There was no correlation between HOVR and any of the correcting factors. To account for disparities in body size, volume-related results were scaled for body weight. The HCVR corrected for weight (HCVR/WT) decreased with age (r = -0.57, P < 0.001). HCVR/WT was significantly higher in children than in adults (0.056 +/- 0.024 vs. 0.032 +/- 0.015 l.kg-1 x min-1. Torr end-tidal PCO2-1, P < 0.001). The (tidal volume/inspiratory duration)/weight, respiratory rate, and heart rate responses to hypercapnia were increased in the children, and the CO2 threshold was lower (36 +/- 5 vs. 40 +/- 6 Torr, P < 0.05). Similarly, the HOVR corrected for weight (HOVR/WT) decreased with age (r = 0.34, P < 0.05), and HOVR/WT was significantly higher in children than in adults (-0.035 +/- 0.017 vs. -0.024 +/- 0.016 l.kg-1 x min-1.% arterial O2 saturation-1, P < 0.02). The respiratory rate and heart rate responses to hypoxia were increased in the children. We conclude that rebreathing HCVR and HOVR are higher during childhood than during adulthood.

Ventilatory Patterns During Hypoxia, Hypercapnia, and Exercise in Adolescents With Mild Scoliosis

PEDIATRICS ◽  
1986 ◽  
Vol 77 (5) ◽  
pp. 692-697
Author(s):  
R. J. Smyth ◽  
K. R. Chapman ◽  
T. A. Wright ◽  
J. S. Crawford ◽  
A. S. Rebuck
Keyword(s):  
Tidal Volume ◽  
Vital Capacity ◽  
Severe Disease ◽  
Pulmonary Mechanics ◽  
Normal Range ◽  
Ventilatory Responses ◽  
Volume Response ◽  
The Mean ◽  
Arterial O2 Saturation ◽  
Maximal Voluntary Ventilation

Adolescents with mild, asymptomatic scoliosis (thoracic curvature &lt;35°) may have little or no impairment of resting lung volumes. Progression to more severe disease may, however, be accompanied by lung restriction, impaired exercise tolerance, and respiratory failure with CO2 retention. We wished to see whether adolescents with mild scoliosis and minimally abnormal resting pulmonary mechanics had impairment of their responses to hypercapnia, hypoxia, and progressive cycle exercise. Forty-four adolescents with idiopathic scoliosis were studied. The mean forced vital capacity (FVC), expressed as a percentage of the predicted value, was 94.3 ± 2.2 (SE). The mean ventilatory response to hypercapnia (2.57 ± 0.24 L/min/mm Hg) was within the normal range but was achieved with a tidal volume response (1.87 ± .17% vital capacity [VC]/mm Hg) that was significantly lower than that previously reported in healthy young adults. Ventilatory responses to exercise were also within the normal range, the mean dyspnea index (VE-max/maximal voluntary ventilation) = 0.92 ± 0.04. However, at a ventilation of 30 L/min, the tidal volume was 0.38 ± 0.01% FVC, which was considerably lower than predicted. The tidal volume response to hypoxia was also abnormally low, the mean response being 0.52 ± 0.059% VC/% decrease in arterial O2 saturation. These findings indicated that, even when scoliosis is asymptomatic and associated with minimal impairment of resting pulmonary function, abnormal patterns of ventilation occur during exercise or in response to chemical stimuli.

Alteration by hyperoxia of ventilatory dynamics during sinusoidal work

1980 ◽  
Vol 48 (6) ◽  
pp. 1083-1091 ◽  
Author(s):  
R. Casaburi ◽  
R. W. Stremel ◽  
B. J. Whipp ◽  
W. L. Beaver ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Work Load ◽  
Cycle Ergometer ◽  
Work Rate ◽  
Phase Lag ◽  
Ventilatory Responses ◽  
Load Tests ◽  
The Mean ◽  
End Tidal ◽  
End Tidal Co2

The effects of hyperoxia on ventilatory and gas exchange dynamics were studied utilizing sinusoidal work rate forcings. Five subjects exercised on 14 occasions on a cycle ergometer for 30 min with a sinusoidally varying work load. Tests were performed at seven frequencies of work load during air or 100% O2 inspiration. From the breath-by-breath responses to these tests, dynamic characteristics were analyzed by extracting the mean level, amplitude of oscillation, and phase lag for each six variables with digital computer techniques. Calculation of the time constant (tau) of the ventilatory responses demonstrated that ventilatory kinetics were slower during hyperoxia than during normoxia (P less than 0.025; avg 1.56 and 1.13 min, respectively). Further, for identical work rate fluctuations, end-tidal CO2 tension fluctuations were increased by hyperpoxia. Ventilation during hyperoxia is slower to respond to variations in the level of metabolically produced CO2, presumably because hyperoxia attenuates carotid body output; the arterial CO2 tension is consequently less tightly regulated.

Time course of augmentation and depression of hypoxic ventilatory responses at altitude

1994 ◽  
Vol 77 (1) ◽  
pp. 313-316 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
P. Bickler
Keyword(s):  
Pulse Oximetry ◽  
Sea Level ◽  
Time Course ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Ventilatory Response ◽  
Set Point ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

Hypoxic ventilatory response (HVR) and hypoxic ventilatory depression (HVD) were measured in six subjects before, during, and after 12 days at 3,810-m altitude (barometric pressure approximately 488 Torr) with and without 15 min of preoxygenation. HVR was tested by 5-min isocapnic steps to 75% arterial O2 saturation measured by pulse oximetry (Spo2) at an isocapnic PCO2 (P*CO2) chosen to set hyperoxic resting ventilation to 140 ml.kg-1.min-1. Hypercapnic ventilatory response (HCVR, 1.min-1.Torr-1) was tested at ambient and high SPO2 6–8 min after a 6- to 10-Torr step increase of end-tidal PCO2 (PETCO2) above P*CO2. HCVR was independent of preoxygenation and was not significantly increased at altitude (when corrected to delta logPCO2). Preoxygenated HVR rose from -1.13 +/- 0.23 (SE) l.min-1.%SPO2(-1) at sea level to -2.17 +/- 0.13 by altitude day 12, without reaching a plateau, and returned to control after return to sea level for 4 days. Ambient HVR was measured at P*CO2 by step reduction of SPO2 from its ambient value (86–91%) to approximately 75%. Ambient HVR slope was not significantly less, but ventilation at equal levels of SPO2 and PCO2 was lower by 13.3 +/- 2.4 l/min on day 2 (SPO2 = 86.2 +/- 2.3) and by 5.9 +/- 3.5 l/min on day 12 (SPO2 = 91.0 +/- 1.5; P < 0.05). This lower ventilation was estimated (from HCVR) to be equivalent to an elevation of the central chemoreceptor PCO2 set point of 9.2 +/- 2.1 Torr on day 2 and 4.5 +/- 1.3 on day 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of acute and chronic acetazolamide on resting ventilation and ventilatory responses in men

1993 ◽  
Vol 74 (1) ◽  
pp. 230-237 ◽  
Author(s):  
E. R. Swenson ◽  
J. M. Hughes
Keyword(s):  
Metabolic Acidosis ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Acidosis ◽  
Acute Effects ◽  
Acid Base Balance ◽  
Ventilatory Control ◽  
Peripheral Chemoreceptor ◽  
Ventilatory Responses ◽  
Base Balance

The effects of acetazolamide (ACTZ) on ventilatory control are thought to be mediated by metabolic acidosis. However, carbonic anhydrase (CA) inhibition within brain and chemoreceptors and tissue respiratory acidosis may also be important. We compared the acute effects of ACTZ (tissue respiratory acidosis and tissue CA inhibition without metabolic acidosis) on ventilation and ventilatory control with chronic ACTZ (acute effects plus metabolic acidosis). Five men were studied 1 h after 500 mg iv ACTZ or 0.9% saline (acute effects) and also after three doses of ACTZ (500 mg po every 6 h; chronic effects). Minute ventilation (VE), steady-state hypercapnic ventilatory response (HCVR), and hypoxic ventilatory response (HVR) were measured with respiratory inductance plethysmography. Resting VE was increased equally by acute and chronic ACTZ. HCVR increased with chronic ACTZ in hyperoxia and even further in hypoxia. In contrast, acute ACTZ had no effect on the HCVR slope in hyperoxia and suppressed its augmentation by hypoxia. HVR was fully suppressed by acute ACTZ but unchanged with chronic ACTZ. ACTZ also slowed the rate of full ventilatory response to CO2. These findings show that CA inhibitors affect ventilatory control in a complex fashion, not only through changes in systemic acid-base balance but also by central and peripheral chemoreceptor inhibition.

scholarly journals Elevated End-Tidal Carbon Monoxide Concentration in Children with Sickle Cell Anemia

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 1390-1390
Author(s):  
Ashutosh Lal ◽  
Kristen Yen ◽  
Lasandra Patterson ◽  
Alisa Goldrich ◽  
Anne M Marsh ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Young Children ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Second Hand Smoke ◽  
Control Group ◽  
Exhaled Breath ◽  
Healthy Children ◽  
The Mean ◽  
End Tidal

Abstract Background: Carbon monoxide (CO) produced during oxygen-dependent cleavage of porphyrin ring of heme is excreted in exhaled breath. The catabolism of heme is increased when red blood cells are destroyed at an accelerated rate. Thus, quantifying CO in exhaled breath could serve as an indicator of hemolysis. However, the requirement for forced breath sample has limited the measurement of exhaled CO in young children. Objective: To assess end-tidal CO concentration (ETCOc) in children with sickle cell anemia (SCA). Design/Methods: ETCOc was measured using the CoSense ETCO Monitor (Capnia Inc. Palo Alto, CA). Children between 5-14 years with SCA (Hb SS) who were not on chronic transfusions were eligible. Healthy children served as age-matched controls. Children with exposure to second-hand smoke, acute respiratory infection or symptomatic asthma were excluded. End-tidal breath samples were collected by placing the tip of a nasal cannula 5 mm into the nares. Up to 3 measurements were taken for each subject and the highest ETCOc value was used for analysis. (ClinicalTrials.gov: NCT01848691) Results: The mean (range) age of 16 children with SCA and 16 controls was 9.7 years (5-14 years) and 9.9 years (5-14 years), respectively. The mean (± s.d.) ETCOc for SCA was 4.85 ± 2.24 ppm versus 0.96 ± 0.54 ppm for control group (p<0.001). The ETCOc in the control group ranged from 0.2 to 2.3 ppm, but was ≤1.2 ppm in 14/16, which is suggested as the upper limit of normal for healthy children. In the SCA group, the ETCOc range was 1.8 to 9.7 ppm, with values ≥2.4 ppm in 15/16 subjects. A threshold ETCOc value of >2.1 ppm provided both sensitivity and specificity equal to 93.8% (69.8-99.8%) for distinguishing SCA from healthy children. Children with SCA who had higher absolute reticulocyte count also demonstrated higher ETCOc (r=0.62, p=0.011). Patients with severe anemia (hemoglobin <8 g/dL) had a higher mean ETCOc (5.43 ppm) than the rest (4.40 ppm) but the difference was not significant. ETCOc level tended to increase with age in SCA (r=0.45, p=0.08). Conclusions: Carbon monoxide in exhaled breath can be measured in young children in the clinic using a portable monitor. ETCOc may be a valuable tool for non-invasive monitoring of the severity of hemolysis in SCA. The mean ETCOc was 5-fold higher in SCA compared with controls, with little overlap seen between the groups. This suggests a potential use for ETCOc as a point-of-care screening test for SCA in children. Figure 1 Figure 1. Figure 2 Figure 2. Disclosures Lal: Capnia, Inc: Research Funding. Yen:Capnia, Inc. : Employment. Bhatnagar:Capnia, Inc: Employment.

Increased chemoreceptor output and ventilatory response to sustained hypoxia

1989 ◽  
Vol 67 (3) ◽  
pp. 1157-1163 ◽  
Author(s):  
D. Georgopoulos ◽  
S. Walker ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Base Line ◽  
Breathing Patterns ◽  
Peripheral Chemoreceptor ◽  
Depressant Action ◽  
Before And After ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

In adult humans the ventilatory response to sustained hypoxia (VRSH) is biphasic, characterized by an initial brisk increase, due to peripheral chemoreceptor (PC) stimulation, followed by a decline attributed to central depressant action of hypoxia. To study the effects of selective stimulation of PC on the ventilatory response pattern to hypoxia, the VRSH was evaluated after pretreatment with almitrine (A), a PC stimulant. Eight subjects were pretreated with A (75 mg po) or placebo (P) on 2 days in a single-blind manner. Two hours after drug administration, they breathed, in succession, room air (10 min), O2 (5 min), room air (5 min), hypoxia [25 min, arterial O2 saturation (SaO2) = 80%], O2 (5 min), and room air (5 min). End-tidal CO2 was kept constant at the normoxic base-line values. Inspiratory minute ventilation (VI) and breathing patterns were measured over the last 2 min of each period and during minutes 3–5 of hypoxia, and nadirs in VI were assessed just before and after O2 exposure. Independent of the day, the VRSH was biphasic. With P and A pretreatment, early hypoxia increased VI 4.6 +/- 1 and 14.2 +/- 1 (SE) l/min, respectively, from values obtained during the preceding room-air period. On A day the hypoxic ventilatory decline was significantly larger than that on P day, and on both days the decline was a constant fraction of the acute hypoxic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory responses to dead space and CO2 breathing under inspiratory resistive load

1995 ◽  
Vol 78 (2) ◽  
pp. 555-561 ◽  
Author(s):  
D. A. Sidney ◽  
C. S. Poon
Keyword(s):  
Breathing Pattern ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Resistive Load ◽  
Healthy Human ◽  
Ventilatory Responses ◽  
Ventilatory Pattern ◽  
Volume Relationship ◽  
The Mean ◽  
End Tidal

To investigate how breathing is controlled during CO2 stimulation, steady-state ventilatory responses to rebreathing through a tube (DS) and inspiring a fixed PCO2 (INH) were compared in healthy human subjects. Tests were performed in hyperoxia with (IRL) and without (NL) an inspiratory resistive load (15 cmH2O.l–1.s at 1 l/s). The mean slope of the minute ventilation (VE)-end-tidal PCO2 relationship was significantly higher in DS-IRL than in INH-IRL [1.86 +/- 0.67 (SD) vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.01], and it was significantly different between INH-NL and INH-IRL (1.64 +/- 0.41 vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.05) but not between DS-NL and DS-IRL (1.85 +/- 0.72 vs. 1.86 +/- 0.67 l.min-1.Torr-1). The slope of the VE-tidal volume relationship was significantly lower in DS-NL than in INH-NL (19.6 +/- 3.8 vs. 21.2 +/- 5.1 min-1, P < 0.05), but other comparisons in breathing pattern between NL and IRL and between DS and INH failed to reach significance. We concluded that 1) alterations in alveolar PCO2 temporal profile by DS could induce changes in VE-end-tidal PCO2 sensitivity and ventilatory pattern, 2) these changes may be modified by increased mechanical impairment resulting from IRL, and 3) carotid chemoreceptor mediation is not necessary for the observed effects of DS.

Sex-related Differences in the Influence of Morphine on Ventilatory Control in Humans 

1998 ◽  
Vol 88 (4) ◽  
pp. 903-913 ◽  
Author(s):  
Albert MD Dahan ◽  
Elise Sarton ◽  
Luc Teppema ◽  
Cees Olievier
Keyword(s):  
Carbon Dioxide ◽  
Carbon Dioxide Tension ◽  
Ventilatory Control ◽  
Double Blind ◽  
Men And Women ◽  
Analgesic Effects ◽  
Ventilatory Responses ◽  
Intravenous Morphine ◽  
End Tidal ◽  
Induced Changes

Background Opiate agonists have different analgesic effects in male and female patients. The authors describe the influence of sex on the respiratory pharmacology of the mu-receptor agonist morphine. Methods The study was placebo-controlled, double-blind, and randomized. Steady-state ventilatory responses to carbon dioxide and responses to a step into hypoxia (duration, 3 min; oxygen saturation, approximately 82%; end-tidal carbon dioxide tension, 45 mmHg) were obtained before and during intravenous morphine or placebo administration (bolus dose of 100 microg/kg, followed by a continuous infusion of 30 microg x kg(-1) x h(-1)) in 12 men and 12 women. Results In women, morphine reduced the slope of the ventilatory response to carbon dioxide from 1.8 +/- 0.9 to 1.3 +/- 0.7 l x min(-1) x mmHg(-1) (mean +/- SD; P &lt; 0.05), whereas in men there was no significant effect (control = 2.0 +/- 0.4 vs. morphine = 1.8 +/- 0.4 l x min(-1) x mmHg(-1)). Morphine had no effect on the apneic threshold in women (control = 33.8 +/- 3.8 vs. morphine = 35.3 +/- 5.3 mmHg), but caused an increase in men from 34.5 +/- 2.3 to 38.3 +/- 3 mmHg, P &lt; 0.05). Morphine decreased hypoxic sensitivity in women from 1.0 +/- 0.5 l x min(-1) x %(-1) to 0.5 +/- 0.4 l x min(-1) x %(-1) (P &lt; 0.05) but did not cause a decrease in men (control = 1.0 +/- 0.5 l x min(-1) x %(-1) vs. morphine = 0.9 +/- 0.5 l x min(-1) x %(-1)). Weight, lean body mass, body surface area, and calculated fat mass differed between the sexes, but their inclusion in the analysis as a covariate revealed no influence on the differences between men and women in morphine-induced changes. Conclusions In both sexes, morphine affects ventilatory control. However, we observed quantitative and qualitative differences between men and women in the way morphine affected the ventilatory responses to carbon dioxide and oxygen. Possible mechanisms for the observed sex differences in the respiratory pharmacology of morphine are discussed.

Ventilatory responses of newborn calves to progressive hypoxia in quiet and active sleep

1980 ◽  
Vol 48 (5) ◽  
pp. 892-895 ◽  
Author(s):  
H. E. Jeffery ◽  
D. J. Read
Keyword(s):  
Ventilatory Response ◽  
Active Sleep ◽  
Sleep State ◽  
Quiet Sleep ◽  
Ventilatory Responses ◽  
Progressive Hypoxia ◽  
Newborn Calves ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
And Behavior

Isocapnic progressive hypoxia was produced by rebreathing 8-10% oxygen in replicate tests during quiet and active sleep, in five full-term calves aged 1-8 days. Airflow through a tightly fitting mask was digitized at 50-ms intervals to calculate breath-by-breath ventilation and rate. Using a cuvette oximeter, arterial O2 saturation (SaO2) was recorded continuously. A mass-spectrometer record of end-tidal PO2 and PCO2 confirmed the mask seal and the constancy of PCO2. Sleep state was characterized by EEG, EOG, neck EMG, and behavior. In quiet sleep the ratio of ventilation to its normoxic control (VR) increased linearly as SaO2 fell; reflex arousal occurred at SaO2 84.9 ± 4.3% (SD) with VR 1.4 ± 0.39 (SD). In contrast, during active sleep, hypoxemia progressed without any ventilatory response to a very low SaO2; a reflex arousal occurred at SaO2 59.2 ±11.0%, often with a ventilatory response developing abruptly just prior to arousal. The slope of the VR/SaO2 regression lines for the overlapping range of SaO2 differed significantly with state in each animal (P < 0.001); the pooled VR values at SaO2 75% were 1.73± 0.15 (SD) and 0.91 ± 0.18 for quiet and active sleep respectively. The depression of the ventilatory response to hypoxia in active sleep differs from previous reports on adult dogs. The basis for this difference needs to be evaluated in relation to species and age, in particular in relation to both the mechanics of breathing and to chemoreceptor reflexes.

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