Influence of passive hyperthermia on human ventilation during rest and isocapnic hypoxia

2007 ◽  
Vol 32 (4) ◽  
pp. 721-732 ◽  
Author(s):  
Andrew N. Curtis ◽  
Michael L. Walsh ◽  
Matthew D. White

The purpose of this study was to examine the potential interaction of core temperature and isocapnic hypoxia on human ventilation and heart rate (HR). In 2 resting head-out water-immersion trials, 8 males first breathed air and then 12% O2 in N2 while the end-tidal partial pressure of carbon dioxide was kept 0.98 (0.66) mmHg (mean (SD)) above normothermic resting levels. The first immersion trial was with a normothermic esophageal temperature (Tes) of ~36.7 °C, and for the second trial, 1 h later, water temperature was increased to give a hyperthermic Tes of ~38.2 °C. Isocapnic hypoxia increased normothermic ventilation by 4 L·min–1 (p = 0.01) from 10.12 (1.07) to 14.20 (3.21) L·min–1, and hyperthermic ventiliation by 7 L·min–1 (p = 0.002) from 13.58 (2.58) to 20.79 (3.73) L·min–1. Ventilation increases during hyperthermia were mediated by breathing frequency and, during isocapnic hypoxia, by tidal volume. Unexpectedly, there was an absence of any hypoxic ventilatory decline that could be attributed to a hydrostatic effect of immersion. Isocapnic hypoxia increased the HR by similar amounts of ~10 and ~11 beats·min–1 in normothermia and hyperthermia, respectively. In conclusion, it appears that hyperthermia increases human ventilatory but not heart rate responses to isocapnic hypoxia.

2014 ◽  
pp. 457-463
Author(s):  
R. AFROUNDEH ◽  
T. ARIMITSU ◽  
R. YAMANAKA ◽  
C. S. LIAN ◽  
K. SHIRAKAWA ◽  
...  

Time delay in the mediation of ventilation (VE) by arterial CO2 pressure (PaCO2) was studied during recovery from short impulse-like exercises with different work loads of recovery. Subjects performed two tests including 10-s impulse like exercise with work load of 200 watts and 15-min recovery with 25 watts in test one and 50 watts in test two. VE, end tidal CO2 pressure (PETCO2) and heart rate (HR) were measured continuously during rest, warming up, exercise and recovery. PaCO2 was estimated from PETCO2 and tidal volume (VT). Results showed that predicted arterial CO2 pressure (PaCO2 pre) increased during recovery in both tests. In both tests, VE increased and peaked at the end of exercise. VE decreased in the first few seconds of recovery but started to increase again. The highest correlation coefficient between PaCO2 pre and VE was obtained in the time delay of 7 s (r=0.854) in test one and in time delays of 6 s (r=0.451) and 31 s (r=0.567) in test two. HR was significantly higher in test two than in test one. These results indicate that PaCO2 pre drives VE with a time delay and that higher work intensity induces a shorter time delay.


PEDIATRICS ◽  
1995 ◽  
Vol 95 (6) ◽  
pp. 864-867
Author(s):  
Janet G. Wingkun ◽  
Janet S. Knisely ◽  
Sidney H. Schnoll ◽  
Gary R. Gutcher

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.


1981 ◽  
Vol 51 (3) ◽  
pp. 654-659 ◽  
Author(s):  
R. B. Banzett ◽  
G. F. Inbar ◽  
R. Brown ◽  
M. Goldman ◽  
A. Rossier ◽  
...  

We recorded the diaphragm electromyogram (EMG) of quadriplegic men before and during exposure of the lower torso to continuous negative pressure, which caused shortening of the inspiratory muscles by expanding the respiratory system by one tidal volume. The moving-time-averaged diaphragm EMG was larger during expansion of the respiratory system. When we repeated the experiment with subjects who breathed through a mouthpiece, we found qualitatively similar EMG changes and little or no change in tidal volume or end-tidal CO2 partial pressure. When the pressure was applied or removed rapidly, changes in EMG occurred within one or two breaths. Because end-tidal CO2 partial pressure did not increase, and because the response was rapid, we suggest that the response results from proprioceptive, rather than chemoreceptive, reflexes. As most of these men had complete spinal lesions at C6 or C7 the afferent pathways are likely to be vagal or phrenic.


1996 ◽  
Vol 6 (2) ◽  
pp. 136-142 ◽  
Author(s):  
Luc Mertens ◽  
Ralph Rogers ◽  
Tony Reybrouck ◽  
Monique Dumoulin ◽  
Luc Vanhees ◽  
...  

AbstractThe purpose of this study was to assess cardiorespiratory responses to submaximal exercise in patients with univentricular atrioventricular connection after the Fontan operation, and to evaluate whether changes occur during medium-term follow-up. Eighteen patients (age 12.1±5.5 years) underwent graded exercise test on a treadmill 2.3±1.4 year after the Fontan repair. Ventilatory gases were measured using breath-by-breath analysis. Results were compared to gender/age-matched controls. Twelve patients (age 14.2±5.4 years) were reevaluated 2.4±2.1 years after the first test. Aerobic exercise performance was subnormal in all patients during the first test. At the lowest level of exercise, the ventilatory threshold was already surpassed in 6/18 patients, while it was reduced in all other patients (p<0.001). All patients were in stable sinus rhythm throughout the test. Heart rate at all exercise levels was ±10% below normal (p<0.05). The respiratory frequency was increased at all exercise levels (p<0.001). The ventilatory equivalent for oxygen was increased (p<0.001), and the end-tidal tension of carbon dioxide was decreased (p<0.001). The ratio of physiological dead space/tidal volume was increased in all patients (p<0.001), while the normal decrease of this ratio during exercise was not observed. Upon reevaluation heart rate, respiratory rate, oxygen uptake, venti latory equivalent for oxygen, end-tidal carbon dioxide tension and physiological dead space did not change signifi cantly. Only a slight further decrease in ventilatory threshold was observed. Aerobic performance after the Fontan procedure ranges widely from just above resting metabolic rate to the lower limit of normal. Dyspnea during exercise is exacerbated by a decreased ventilatory threshold, increased physiological dead space, and decreased respir-atory efficiency. Cardiorespiratory response to exercise, nonetheless, remains relatively stable during medium-term follow-up.


1995 ◽  
Vol 82 (2) ◽  
pp. 331-343 ◽  
Author(s):  
David D. Hood ◽  
James C. Eisenach ◽  
Robin Tuttle

Background In dogs, sheep, and rats, spinal neostigmine produces analgesia alone and enhances analgesia from alpha 2-adrenergic agonists. This study assesses side effects and analgesia from intrathecal neostigmine in healthy volunteers. Methods After institutional review board approval and informed consent, 28 healthy volunteers were studied. The first 14 volunteers received neostigmine (50-750 micrograms) through a #19.5 spinal needle followed by insertion of a spinal catheter. The remaining 14 volunteers received neostigmine through a #25 or #27 spinal needle without a catheter. Safety measurements included blood pressure, heart rate, oxyhemoglobin saturation, end-tidal carbon dioxide, neurologic evaluation, and computer tests of vigilance and memory. Analgesia in response to ice water immersion was measured. Results Neostigmine (50 micrograms) through the #19.5 needle did not affect any measured variable. Neostigmine (150 micrograms) caused mild nausea, and 500-750 micrograms caused severe nausea and vomiting. Neostigmine (150-750 micrograms) produced subjective leg weakness, decreased deep tendon reflexes, and sedation. The 750-micrograms dose was associated with anxiety, increased blood pressure and heart rate, and decreased end-tidal carbon dioxide. Neostigmine (100-200 micrograms) in saline, injected through a #25 or #27 needle, caused protracted, severe nausea, and vomiting. This did not occur when dextrose was added to neostigmine. Neostigmine by either method of administration reduced visual analog pain scores to immersion of the foot in ice water. Conclusions The incidence and severity of these adverse events from intrathecal neostigmine appears to be affected by dose, method of administration, and baricity of solution. These effects in humans are consistent with studies in animals. Because no unexpected or dangerous side effects occurred, cautious examination of intrathecal neostigmine alone and in combination with other agents for analgesia is warranted.


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