Decreased Carbon Dioxide Sensitivity in Infants of Substance-Abusing Mothers

PEDIATRICS ◽  
1995 ◽  
Vol 95 (6) ◽  
pp. 864-867
Author(s):  
Janet G. Wingkun ◽  
Janet S. Knisely ◽  
Sidney H. Schnoll ◽  
Gary R. Gutcher
Keyword(s):  
Carbon Dioxide ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Demographic Data ◽  
Substance Abusing ◽  
Quiet Sleep ◽  
Co2 Level ◽  
The Difference ◽  
End Tidal ◽  
Drug Free

Objective. To determine whether there is a demonstrable abnormality in control of breathing in infants of substance-abusing mothers during the first few days of life. Methods. We enrolled 12 drug-free control infants and 12 infants of substance abusing mothers (ISAMs). These infants experienced otherwise uncomplicated term pregnancies and deliveries. The infants were assigned to a group based on the results of maternal histories and maternal and infant urine toxicology screens. Studies were performed during quiet sleep during the first few days of life. We measured heart rate, oxygen saturations via a pulse oximeter, end-tidal carbon dioxide (ET-CO2) level, respiratory rate, tidal volume, and airflow. The chemoreceptor response was assessed by measuring minute ventilation and the ET-CO2 level after 5 minutes of breathing either room air or 4% carbon dioxide. Results. The gestational ages by obstetrical dating and examination of the infants were not different, although birth weights and birth lengths were lower in the group of ISAMs. Other demographic data were not different, and there were no differences in the infants' median ages at the time of study or in maternal use of tobacco and alcohol. The two groups had comparable baseline (room air) ET-CO2 levels, respiratory rates, tidal volumes, and minute ventilation. When compared with the group of ISAMs, the drug-free group had markedly increased tidal volume and minute ventilation on exposure to 4% carbon dioxide. These increases accounted for the difference in sensitivity to carbon dioxide, calculated as the change in minute ventilation per unit change in ET-CO2 (milliliters per kg/min per mm Hg). The sensitivity to carbon dioxide of control infants was 48.66 ± 7.14 (mean ± SE), whereas that of ISAMs was 16.28 ± 3.14. Conclusions. These data suggest that ISAMs are relatively insensitive to challenge by carbon dioxide during the first few days of life. We speculate that this reflects an impairment of the chemoreceptor response.

Ventilatory response to hypoxia in unanesthetized newborn kittens

1988 ◽  
Vol 64 (6) ◽  
pp. 2544-2551 ◽  
Author(s):  
H. Rigatto ◽  
C. Wiebe ◽  
C. Rigatto ◽  
D. S. Lee ◽  
D. Cates
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Quiet Sleep ◽  
Newborn Kitten ◽  
Peripheral Mechanism ◽  
Flow Through ◽  
Ventilatory Response To Hypoxia

We studied the ventilatory response to hypoxia in 11 unanesthetized newborn kittens (n = 54) between 2 and 36 days of age by use of a flow-through system. During quiet sleep, with a decrease in inspired O2 fraction from 21 to 10%, minute ventilation increased from 0.828 +/- 0.029 to 1.166 +/- 0.047 l.min-1.kg-1 (P less than 0.001) and then decreased to 0.929 +/- 0.043 by 10 min of hypoxia. The late decrease in ventilation during hypoxia was related to a decrease in tidal volume (P less than 0.001). Respiratory frequency increased from 47 +/- 1 to 56 +/- 2 breaths/min, and integrated diaphragmatic activity increased from 14.9 +/- 0.9 to 20.2 +/- 1.4 arbitrary units; both remained elevated during hypoxia (P less than 0.001). Younger kittens (less than 10 days) had a greater decrease in ventilation than older kittens. These results suggest that the late decrease in ventilation during hypoxia in the newborn kitten is not central but is due to a peripheral mechanism located in the lungs or respiratory pump and affecting tidal volume primarily. We speculate that either pulmonary bronchoconstriction or mechanical uncoupling of diaphragm and chest wall may be involved.

Ventilatory responses to carbon dioxide at low and high levels of oxygen are elevated after episodic hypoxia in men compared with women

2004 ◽  
Vol 97 (5) ◽  
pp. 1673-1680 ◽  
Author(s):  
Chris Morelli ◽  
M. Safwan Badr ◽  
Jason H. Mateika
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
High Oxygen ◽  
Set Point ◽  
Ventilatory Responses ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Oxygen Gas ◽  
End Tidal

We hypothesized that the acute ventilatory response to carbon dioxide in the presence of low and high levels of oxygen would increase to a greater extent in men compared with women after exposure to episodic hypoxia. Eleven healthy men and women of similar race, age, and body mass index completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the end-tidal partial pressure of carbon dioxide (PetCO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr), or high oxygen gas mixture (150 Torr). During the trials, PetCO2 increased while the selected level of oxygen was maintained. The point at which minute ventilation began to rise in a linear fashion as PetCO2 increased was considered to be the carbon dioxide set point. The ventilatory response below and above this point was determined. The results showed that the ventilatory response to carbon dioxide above the set point was increased in men compared with women before exposure to episodic hypoxia, independent of the oxygen level that was maintained during the rebreathing trials (50 Torr: men, 5.19 ± 0.82 vs. women, 4.70 ± 0.77 l·min−1·Torr−1; 150 Torr: men, 4.33 ± 1.15 vs. women, 3.21 ± 0.58 l·min−1·Torr−1). Moreover, relative to baseline measures, the ventilatory response to carbon dioxide in the presence of low and high oxygen levels increased to a greater extent in men compared with women after exposure to episodic hypoxia (50 Torr: men, 9.52 ± 1.40 vs. women, 5.97 ± 0.71 l·min−1·Torr−1; 150 Torr: men, 5.73 ± 0.81 vs. women, 3.83 ± 0.56 l·min−1·Torr−1). Thus we conclude that enhancement of the acute ventilatory response to carbon dioxide after episodic hypoxia is sex dependent.

scholarly journals Increased vasoconstriction predisposes to hyperpnea and postural faint

2008 ◽  
Vol 295 (1) ◽  
pp. H372-H381 ◽  
Author(s):  
Indu Taneja ◽  
Marvin S. Medow ◽  
June L. Glover ◽  
Neeraj K. Raghunath ◽  
Julian M. Stewart
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Peripheral Resistance ◽  
Impedance Plethysmography ◽  
Blood Flows ◽  
Control Subjects ◽  
Regional Blood Flows ◽  
Healthy Control ◽  
End Tidal ◽  
Upright Tilt

Our prior studies indicated that postural fainting relates to splanchnic hypervolemia and thoracic hypovolemia during orthostasis. We hypothesized that thoracic hypovolemia causes excessive sympathetic activation, increased respiratory tidal volume, and fainting involving the pulmonary stretch reflex. We studied 18 patients 13–21 yr old, 11 who fainted within 10 min of upright tilt (fainters) and 7 healthy control subjects. We measured continuous blood pressure and heart rate, respiration by inductance plethysmography, end-tidal carbon dioxide (ETCO2) by capnography, and regional blood flows and blood volumes using impedance plethysmography, and we calculated arterial resistance with patients supine and during 70° upright tilt. Splanchnic resistance decreased until faint in fainters (44 ± 8 to 21 ± 2 mmHg·l−1·min−1) but increased in control subjects (47 ± 5 to 53 ± 4 mmHg·l−1·min−1). Percent change in splanchnic blood volume increased (7.5 ± 1.0 vs. 3.0 ± 11.5%, P < 0.05) after the onset of tilt. Upright tilt initially significantly increased thoracic, pelvic, and leg resistance in fainters, which subsequently decreased until faint. In fainters but not control subjects, normalized tidal volume (1 ± 0.1 to 2.6 ± 0.2, P < 0.05) and normalized minute ventilation increased throughout tilt (1 ± 0.2 to 2.1 ± 0.5, P < 0.05), whereas respiratory rate decreased (19 ± 1 to 15 ± 1 breaths/min, P < 0.05). Maximum tidal volume occurred just before fainting. The increase in minute ventilation was inversely proportionate to the decrease in ETCO2. Our data suggest that excessive splanchnic pooling and thoracic hypovolemia result in increased peripheral resistance and hyperpnea in simple postural faint. Hyperpnea and pulmonary stretch may contribute to the sympathoinhibition that occurs at the time of faint.

Computer-based system for analysis of respiratory responses to exercise

1977 ◽  
Vol 42 (6) ◽  
pp. 968-975 ◽  
Author(s):  
D. H. Pearce ◽  
H. T. Milhorn ◽  
G. H. Holloman ◽  
W. J. Reynolds
Keyword(s):  
Carbon Dioxide ◽  
Respiratory Exchange Ratio ◽  
Minute Ventilation ◽  
Type System ◽  
Work Load ◽  
Magnetic Type ◽  
Computer Based ◽  
End Tidal ◽  
Good Agreement

A computer-based system for the determination of tidal volume, respiratory frequency, minute ventilation, oxygen transfer, carbon dioxide transfer, respiratory exchange ratio, end-tidal oxygen, end-tidal carbon dioxide, and heart rate is presented. These variables are first determined on a breath-by-breath basis from data (expired carbon dioxide and oxygen fractions, airflow, and ECG) prerecorded on an FM magnetic type system. The breath-by-breath data are then averaged for each experimental run in 5-s increments. The 5-s increment data from a group of subjects can then be averaged and the SEM determined at prescribed periods of time. For the study of individual respiratory transient we found the 5-s increment data to be more useful than the breath-by-breath data because it has a lesser degree of fluctuation. The system is especially adapted to careful observation of the responses within the first few seconds of a change in work load. Appropriate computer programs are discussed. The results of several experiments are compared with data from other sources and found to be in good agreement.

Ventilatory Responses to Exercise and to Carbon Dioxide in Mitral Stenosis before and after Valvulotomy: Causes of Tachypnoea

1978 ◽  
Vol 54 (1) ◽  
pp. 9-16 ◽  
Author(s):  
J. W. Reed ◽  
M. Ablett ◽  
J. E. Cotes
Keyword(s):  
Carbon Dioxide ◽  
Tidal Volume ◽  
Mitral Stenosis ◽  
Vital Capacity ◽  
Minute Ventilation ◽  
Residual Effect ◽  
Minute Volume ◽  
Cardiac Frequency ◽  
Control Subjects ◽  
Exercise Ventilation

1. The ventilation and cardiac frequency during progressive exercise and the respiratory responses to breathing carbon dioxide have been measured in 33 female patients with mitral stenosis and in 31 control subjects. Compared with the control subjects, the patients' exercise ventilation and cardiac frequency were increased; the exercise tidal volume at standard minute volume, the vital capacity and the ventilatory response to carbon dioxide were reduced. The extent to which the standardized tidal volume was lower during exercise than during breathing carbon dioxide was correlated with the severity of the stenosis, as gauged by the increase in exercise cardiac frequency above the level predicted from anthropometric measurements. 2. Twenty patients were studied postoperatively. In the 12 who showed clinical improvement the exercise ventilation and cardiac frequency were reduced and the exercise tidal volume at a given minute ventilation was increased. The latter change occurred despite a reduction in vital capacity, which was probably a residual effect of thoractomy. There was no significant change in the response to breathing carbon dioxide. No material change in function was observed in the patients whose condition was not improved by the operation. 3. It is suggested that in mitral stenosis the tachypnoea which occurs during exercise, whilst mainly a mechanical consequence of the reduced vital, capacity, is also partly due to pulmonary congestion stimulating intrapulmonary receptors.

Effects of elevated oxygen and carbon dioxide partial pressures on respiratory function and cognitive performance

2014 ◽  
Vol 117 (4) ◽  
pp. 406-412 ◽  
Author(s):  
Matthew Gill ◽  
Michael J. Natoli ◽  
Charles Vacchiano ◽  
David B. MacLeod ◽  
Keita Ikeda ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Respiratory Function ◽  
Vision Loss ◽  
Minute Ventilation ◽  
Cycle Ergometer ◽  
Hyperbaric Chamber ◽  
Tunnel Vision ◽  
Partial Pressures ◽  
Ergometer Exercise ◽  
End Tidal

Hyperoxia during diving has been suggested to exacerbate hypercapnic narcosis and promote unconsciousness. We tested this hypothesis in male volunteers (12 at rest, 10 at 75 W cycle ergometer exercise) breathing each of four gases in a hyperbaric chamber. Inspired Po2 (PiO2) was 0.21 and 1.3 atmospheres (atm) without or with an individual subject's maximum tolerable inspired CO2 (PiO2 = 0.055–0.085 atm). Measurements included end-tidal CO2 partial pressure (PetCO2), rating of perceived discomfort (RPD), expired minute ventilation (V̇e), and cognitive function assessed by auditory n-back test. The most prominent finding was, irrespective of PetCO2, that minute ventilation was 8–9 l/min greater for rest or exercise with a PiO2 of 1.3 atm compared with 0.21 atm ( P < 0.0001). For hyperoxic gases, PetCO2 was consistently less than for normoxic gases ( P < 0.01). For hyperoxic hypercapnic gases, n-back scores were higher than for normoxic gases ( P < 0.01), and RPD was lower for exercise but not rest ( P < 0.02). Subjects completed 66 hyperoxic hypercapnic trials without incident, but five stopped prematurely because of serious symptoms (tunnel vision, vision loss, dizziness, panic, exhaustion, or near syncope) during 69 normoxic hypercapnic trials ( P = 0.0582). Serious symptoms during hypercapnic trials occurred only during normoxia. We conclude serious symptoms with hyperoxic hypercapnia were absent because of decreased PetCO2 consequent to increased ventilation.

Noninvasive, Automated and Continuous Cardiac Output Monitoring by Pulmonary Capnodynamics

2006 ◽  
Vol 105 (1) ◽  
pp. 72-80 ◽  
Author(s):  
Philip J. Peyton ◽  
Yagnaprabhu Venkatesan ◽  
Sally G. Hood ◽  
Paul Junor ◽  
Clive May
Keyword(s):  
Carbon Dioxide ◽  
Cardiac Output ◽  
Critical Care ◽  
Major Surgery ◽  
Cardiac Output Monitoring ◽  
Flow Probe ◽  
Routine Basis ◽  
The Difference ◽  
Output Monitoring ◽  
End Tidal

Background Cardiac output monitoring is most important where cardiovascular stability is potentially threatened, such as during major surgery and in critically ill patients. However, continuous monitoring of cardiac output is still not performed routinely during anesthesia and critical care, because of invasiveness, expense, and inaccuracy of available technologies. Methods A technique termed the capnodynamic method was tested for breath-to-breath measurement of pulmonary blood flow from lung carbon dioxide mass balance, using measured carbon dioxide elimination and end-tidal concentration. A prototype measurement system was constructed for a feasibility study in six anesthetized sheep. Large and rapid fluctuations in cardiac output were generated by repeated dobutamine and esmolol challenge. Measurements were compared with an indwelling ultrasonic flow probe placed on the ascending aorta or pulmonary artery. Results Cardiac output measured by the flow probe varied between zero and 8.67 l/min, with a mean of 3.50 l/min. Overall mean bias [SD of the difference] between the methods (capnodynamic - flow probe) was -0.25 [0.94] l/min, r = 0.79 (P &lt; 0.001). During periods of stability in cardiac output of 5 min or more, mean bias was -0.20 [0.55] l/min. The method successfully indicated two cardiac arrest events, which were induced in one of the animals. Conclusions The method satisfactorily tracked wide fluctuations in cardiac output in real time. The capnodynamic method may have potential for continuous noninvasive cardiac output monitoring in patients undergoing anesthesia for major surgery, and in critical care, on a routine basis.

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