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Relevant bibliographies by topics / Respiration Blood gases

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Academic literature on the topic 'Respiration Blood gases'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Respiration Blood gases"

1

Riley, R. L., R. E. Dutton, F. J. D. Fuleihan, S. Nath, H. H. Hurt, C. Yoshimoto, J. H. Sipple, S. Permutt, and B. Bromberger-Barnea. "REGULATION OF RESPIRATION AND BLOOD GASES*." Annals of the New York Academy of Sciences 109, no. 2 (December 15, 2006): 829–51. http://dx.doi.org/10.1111/j.1749-6632.1963.tb13509.x.

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2

Franklin, Karl A., Erik Sandström, Göran Johansson, and Eva M. Bålfors. "Hemodynamics, cerebral circulation, and oxygen saturation in Cheyne-Stokes respiration." Journal of Applied Physiology 83, no. 4 (October 1, 1997): 1184–91. http://dx.doi.org/10.1152/jappl.1997.83.4.1184.

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Franklin, Karl A., Erik Sandström, Göran Johansson, and Eva M. Bålfors. Hemodynamics, cerebral circulation, and oxygen saturation in Cheyne-Stokes respiration. J. Appl. Physiol. 83(4): 1184–1191, 1997.—Because cardiovascular disorders and stroke may induce Cheyne-Stokes respiration, our purpose was to study the interaction among cerebral activity, cerebral circulation, blood pressure, and blood gases during Cheyne-Stokes respiration. Ten patients with heart failure or a previous stroke were investigated during Cheyne-Stokes respiration with recordings of daytime polysomnography, cerebral blood flow velocity, intra-arterial blood pressure, and intra-arterial oxygen saturation with and without oxygen administration. There were simultaneous changes in wakefulness, cerebral blood flow velocity, and respiration with accompanying changes in blood pressure and heart rate ∼10 s later. Cerebral blood flow velocity, blood pressure, and heart rate had a minimum occurrence in apnea and a maximum occurrence during hyperpnea. The apnea-induced oxygen desaturations were diminished during oxygen administration, but the hemodynamic alterations persisted. Oxygen desaturations were more severe and occurred earlier according to intra-arterial measurements than with finger oximetry. It is not possible to explain Cheyne-Stokes respiration by alterations in blood gases and circulatory time alone. Cheyne-Stokes respiration may be characterized as a state of phase-linked cyclic changes in cerebral, respiratory, and cardiovascular functions probably generated by variations in central nervous activity.

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3

PIVARNIK, JAMES M., WESLEY LEE, THOMAS SPILLMAN, STEVEN L. CLARK, DAVID B. COTTON, and JOANNA F. MILLER. "Maternal respiration and blood gases during aerobic exercise performed at moderate altitude." Medicine & Science in Sports & Exercise 24, no. 8 (August 1992): 868???872. http://dx.doi.org/10.1249/00005768-199208000-00007.

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4

Kline, David D., Tianen Yang, Daniel R. D. Premkumar, Agnes J. Thomas, and Nanduri R. Prabhakar. "Blunted respiratory responses to hypoxia in mutant mice deficient in nitric oxide synthase-3." Journal of Applied Physiology 88, no. 4 (April 1, 2000): 1496–508. http://dx.doi.org/10.1152/jappl.2000.88.4.1496.

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In the present study, the role of nitric oxide (NO) generated by endothelial nitric oxide synthase (NOS-3) in the control of respiration during hypoxia and hypercapnia was assessed using mutant mice deficient in NOS-3. Experiments were performed on awake and anesthetized mutant and wild-type (WT) control mice. Respiratory responses to 100, 21, and 12% O2and 3 and 5% CO2-balance O2were analyzed. In awake animals, respiration was monitored by body plethysmography along with O2consumption (V˙o2) and CO2production (V˙co2). In anesthetized, spontaneously breathing mice, integrated efferent phrenic nerve activity was monitored as an index of neural respiration along with arterial blood pressure and blood gases. Under both experimental conditions, WT mice responded with greater increases in respiration during 12% O2than mutant mice. Respiratory responses to hyperoxic hypercapnia were comparable between both groups of mice. Arterial blood gases, changes in blood pressure,V˙o2, andV˙co2during hypoxia were comparable between both groups of mice. Respiratory responses to cyanide and brief hyperoxia were attenuated in mutant compared with WT mice, indicating reduced peripheral chemoreceptor sensitivity. cGMP levels in the brain stem during 12% O2, taken as an index of NO production, were greater in mutant compared with WT mice. These observations demonstrate that NOS-3 mutant mice exhibit selective blunting of the respiratory responses to hypoxia but not to hypercapnia, which in part is due to reduced peripheral chemosensitivity. These results support the idea that NO generated by NOS-3 is an important physiological modulator of respiration during hypoxia.

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Shams, H., and P. Scheid. "Respiration and blood gases in the duck exposed to normocapnic and hypercapnic hypoxia." Respiration Physiology 67, no. 1 (January 1987): 1–12. http://dx.doi.org/10.1016/0034-5687(87)90002-8.

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6

Khalifa, Mohammed S., Reda H. Kamel, Mona Abu Zikry, and Tarek M. Kandil. "Effect of enlarged adenoids on arterial blood gases in children." Journal of Laryngology & Otology 105, no. 6 (June 1991): 436–38. http://dx.doi.org/10.1017/s0022215100116238.

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AbstractThe enlarged adenoid is a common disorder in children resulting in nasopharyngeal obstruction. Many authors suggest that increased nasal resistance to respiration may cause disturbances in the pulmonary ventilation and carry the risk of obstructive sleep apnoea and/or cardiopulmonary syndrome.This study comprised 30 children complaining of long-standing nasal obstruction due to enlarged adenoids. Adenoidectomy was performed and the arterial blood gases were measured before and one month after surgery. Twelve normal children were also included as controls. Statistical evaluation of the results showed that O2 saturation and arterial O2 tension (PaO2) were significantly low before the operation, and increased significantly after surgery. Arterial CO2 tension (PaCO2) was insignificantly low before operation, but decreased significantly after adenoidectomy. It was concluded that enlarged adenoid may be associated with ventilatory impairment which is reversible after adenoidectomy.

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7

Sanocka, U. M., D. F. Donnelly, and G. G. Haddad. "Autoresuscitation: a survival mechanism in piglets." Journal of Applied Physiology 73, no. 2 (August 1, 1992): 749–53. http://dx.doi.org/10.1152/jappl.1992.73.2.749.

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Piglets were studied to determine 1) the cardiovascular and neurophysiological effects of prolonged laryngeal-induced respiratory inhibition (n = 7) and 2) whether these effects were modulated by autonomic blockade (n = 6). Respiration, electrocardiogram, electroencephalogram (EEG), and blood pressure were recorded, and blood gases were measured. During continuous laryngeal stimulation in the presence of light anesthesia, apnea was interrupted every 1–2.5 min by clusters of two to six breaths. Compared with control, these breaths had a significantly greater tidal volume (430 +/- 30% of control), shorter inspiratory time (87 +/- 5%), and longer expiratory time (124 +/- 15%) and, thus, were of a gasping nature. With each cluster of gasps, arterial PO2 increased from 15 +/- 2 to 56 +/- 5 Torr, heart rate from 84 +/- 7 to 161 +/- 5 beats/min, and mean blood pressure from 48 +/- 4 to 106 +/- 6 mmHg. The EEG became flat by 1 min after the onset of apnea and remained isoelectric throughout the stimulus period. Cyclical gasps were not affected by sympathetic or parasympathetic blockade. These data show that, despite EEG silence, piglets can autoresuscitate by initiating gasps that are not dependent on autonomic integrity. These gasps markedly improve cardiovascular status and may sustain animals for a prolonged period of time.

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8

Peeters, M. E., D. Gil, E. Teske, V. Eyzenbach, W. E. v. d. Brom, J. T. Lumeij, and H. W. de Vries. "Four methods for general anaesthesia in the rabbit: a comparative study." Laboratory Animals 22, no. 4 (October 1, 1988): 355–60. http://dx.doi.org/10.1258/002367788780746197.

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The efficacy and safety of pentobarbitone, ketamine/xylazine, fentanyl/fluanisone/diazepam, and halothane/nitrous oxide anaesthesia were compared in 4 groups of six New Zealand White rabbits. Heart and respiratory rates, body temperature, reflexes, blood pressure and blood gases were measured. Pentobarbitone appeared to be unsuitable for anaesthesia in rabbits, as 5 of the 6 rabbits to whom it was administered, required artificial respiration or died. The combinations of ketamine/xylazine and fentanyl-f1uanisone/diazepam both produced unpredictable levels of anaesthesia together with a substantial decline in arterial blood pressure and Po2. Despite a severe drop in blood pressure (up to 37·5%), anaesthesia with halothane and nitrous oxide was found to be superior to the other anaesthetic agents.

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9

Glass, M. L., R. G. Boutilier, and N. Heisler. "Effects of Body Temperature on Respiration, Blood Gases and Acid-Base Status in the Turtle Chrysemys Picta Bellii." Journal of Experimental Biology 114, no. 1 (January 1, 1985): 37–51. http://dx.doi.org/10.1242/jeb.114.1.37.

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Freshwater turtles (Chrysemys picta bellii Gray) were acclimated to temperatures of 5, 10, 20 and 30°C for at least 12 days, and pulmonary ventilation, oxygen uptake and arterial pH, PCOCO2 and POO2 were determined in completely unrestrained specimens. Oxygen uptake (V·OO2) increased overproportionately (6.7-fold) as compared to pulmonary ventilation (V·1, 4.4-fold) when the temperature increased from 10 to 30°C. The observed rise in arterial PCOCO2 from 13 (5°C) to 32mmHg (30°C) was the result of a decrease in V·1/V·OO2, whereas an increase of arterial POO2 from 12Torr at 5°C to about 60Torr at 20 and 30°C mainly resulted from the effects of intracardiac blood shunting combined with temperature-dependent shifts of the oxygen dissociation curve. Arterial pH fell with rising temperature significantly less (ΔpH/Δt =−0.010U/°C) than required for constant relative alkalinity and for constant dissociation of imidazole. The changes of cerebrospinal fluid pH with temperature, calculated from the mean arterial PCOCO2 values, were even smaller [ΔpH/ΔtCSF = −0.008). It is concluded that the observed temperature dependence of the acid-base status is not in agreement with the alphastat hypothesis.

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10

Miyamura, Miharu, Kinya Nishimura, Koji Ishida, Keisho Katayama, Midori Shimaoka, and Shuichi Hiruta. "Is Man Able to Breathe Once a Minute for an Hour?: The Effect of Yoga Respiration on Blood Gases." Japanese Journal of Physiology 52, no. 3 (2002): 313–16. http://dx.doi.org/10.2170/jjphysiol.52.313.

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Dissertations / Theses on the topic "Respiration Blood gases"

1

Kinker, James Robert. "The effects of pursed-lip breathing and added expiratory resistances on arterialized-venous blood gases and lactic acid /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487266011223814.

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2

Hopkins, Susan Roberta. "The relationship between the hypoxic ventilatory response and arterial desaturation during heavy work." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28535.

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Arterial desaturation in fit athletes, during exercise at an intensity greater than or equal to 90% of VO₂ max has been reported by a number of authors yet the etiology of these changes remain obscure. Inadequate pulmonary ventilation due to a blunted respiratory drive, or lung mechanics has been implicated as a factor in the etiology of this phenomenon. It was the purpose of this experiment to investigate the relationship between arterial desaturation and ventilatory response to hypoxia (HVR). Twelve healthy male subjects ( age = 23.8 ± 3.6 yrs., height = 181.6 ±₋₁ 5.6 cms., Weight = 73.7 ± 6.2 kg., VO₂ max = 63.2 ± 2.2 ml .kg . -1 2 .min⁻¹) performed a five minute exercise test on a treadmill at 100% of VO₂ max. Arterial samples for pH, PCO₂, PO₂, and SaO₂ were withdrawn via an indwelling arterial cannula at rest and every 15s throughout the exercise test. The blood gas samples were analyzed with an Instrument Laboratories 1306 blood gas analyzer. Ventilation and VO₂ were measured by a Beckman metabolic measurement cart. On a separate occasion the ventilatory response to hypoxia (HVR) was determined by recording VE as progressive hypoxia was induced by adding N₂ to a mixing chamber. SaO₂ was measured using a Hewlett-Packard ear oximeter; to maintain isocapnia small ammounts of CO₂ were added to the open circuit system. ANOVA for repeated measured was used to evaluate changes in blood gases, ventilation, and VO₂. Simple linear regression and multiple linear regression was used to evaluate the relationship between the changes in SaO₂ and HVR and the descriptive variables. Subjects showed a significant decline in arterial saturation and PO₂ over the course of the test (p < 0.01,and p < 0.01). Four subjects (Mild) exhibited modest decreases in SaO₂ to (94.6 ± 1.9%), three (Moderate) showed an intermediate response (SaO₂ 91.6 ± 0.1%) and five (Marked) demonstrated a marked decrease in arterial saturation (SaO₂ = 90.0 + 1.2%). The differences in PO₂ and SaO₂ between Mild and Marked groups were significant ( p < 0.05, and p < 0.01); there were no significant differences between groups in VE, VO₂, pH or PCO . There was no significant correlation between the lowest SaO₂ reached and HVR, or any of the descriptive variables. Nine subjects did not reach maximal VE (as determined by the VO₂ max test) on the exercise test, two subjects 2 exhibited similar ventilation, and the remaining subject exceeded maximal VE, but fell into the Mild group with respect to desaturation. Oxygen uptake exceeded that recorded for the VO₂ max determination for four of the five subjects in the Marked group; the remaining subjects demonstrated lower or similar values. It was concluded that arterial desaturation was not related to blunted hypoxic drive.
Education, Faculty of
Curriculum and Pedagogy (EDCP), Department of
Graduate

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3

Roussel, Olivier. "Contribution à l'étude de la morbi-mortalité lors de l'usage de drogues récréatives : GHB-THC, seuls ou associés à l'éthanol." Phd thesis, Université René Descartes - Paris V, 2012. http://tel.archives-ouvertes.fr/tel-00781683.

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L'objectif de cette thèse est de détailler les effets respiratoires induits par les associations de l'éthanol au THC et de l'éthanol au GHB. Les études ont été menées chez l'animal non anesthésié par pléthysmographie corps entier pendant les quatre heures suivant l'administration intrapéritonéale. Dans une première étape, les effets respiratoires de la prise isolée d'éthanol et de GHB ont été étudiés. Ces deux substances modifient le mode respiratoire : l'éthanol provoquant une tachypnée dès 3 g.kg-1, le GHB une respiration apneustique dès 600 mg.kg-1, sans insuffisance respiratoire (PaO2 normale). Les modifications des gaz du sang observées : acidémie pour l'éthanol et alcalose pour le GHB sont d'origine métabolique. A ces doses, ces deux substances perturbent aussi la conscience des animaux et la thermorégulation : l'éthanol induit une hypothermie et le GHB une évolution triphasique de la température : hypothermie/hyperthermie/ hypothermie. Les dosages sanguins et les études cinétiques menés lors de ces études confirment la vraisemblance de notre modèle et sa pertinence clinique et médicolégale. L'étude des associations à l'éthanol montre que les effets respiratoires du THC et du GHB sont conservés, seule leur association à la dose de 3 g.kg-1 d'éthanol a provoqué une baisse de la ventilation minute avec réduction du débit inspiratoire mais selon des mécanismes différents : baisse du volume courant pour l'association THC-éthanol et augmentation de la durée des apnées expiratoires pour celle du GHB à l'éthanol. Pour cette dernière, l'interaction cinétique observée après administration intrapéritonéale n'explique pas l'intensité du phénomène, une potentialisation est probable.

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4

Hopkins, Susan R. "Pulmonary diffusion limitation, V̇ /Q̇ mismatch and pulmonary transit time in highly trained athletes during maximal exercise." Thesis, 1992. http://hdl.handle.net/2429/2620.

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To investigate the relationship between pulmonary diffusion limitation, ventilation-perfusion (VA/Q) mismatch, pulmonary transit times (PTT) and pulmonary gas exchange during exercise, 10 highly trained male athletes (age=26.4±4.4 years, Height=185.5±5.3cms, Weight=78.2±8.6 kg, V 02max=5.15±0.521-min-1) under went exercise testing at rest (R) and 150W, 300W and maximal exercise (372±22W), corresponding to an oxygen consumption (V0₂) of 0.41±0.09, 2.16±0.17, 4.32±0.35 and 5.13±0.50 1-min-1respectively, while trace amounts of six inert gases were infused via a peripheral vein. Arterial blood samples, mixed expired gas samples and metabolic data were obtained. Observed alveolar arterial difference ([A-a]D0₂(0)was calculated according to the alveolar gas equation. Indices of VA/Q mismatch: LogSDi and Log SDa and predicted [A-a]D0₂([A-a]DO₂(p)) were derived from 50 compartment model analysis of retentions and excretions of the inert gases. Additional indices of '/A/I,) mismatch: DISPR*, DISPE and DISPR*_E and inert gas alveolar difference ([A-a]D, R(A-a)D and E(A-a)D) were obtained directly from the inert gas data. One to two weeks later, the subjects underwent first pass radionuclide angiography using a Siemens ZLC wide field of view gamma camera. Following in vitro labeling with 99mTechnecium, 5-10 ml of the subject's blood, containing 10-20 mCi of activity, were injected at rest. First pass and post-static data were obtained on an ADAC 3003 computer and cardiac output was calculated using the Stewart Hamilton equation. PTT was determined using deconvolution and centroid methods. Gated radionuclide angiography was then performed at rest, 150, and 300W. On a separate occasion, first pass cardiac outputs and pulmonary transit times were obtained at maximal exercise. Mean arterial partial pressure of 0₂ (Pa0₂) decreased significantly from rest to 150W , and from 150 to 300W to a low value of 86±9 torn, before increasing to near resting values at maximal exercise. [A-a]D0₂(3) increased across each exercise levels however only the increase from 150 to 300 W was significant. The overall and perfusion-related indices of VA/Q mismatch showed a significant increase with exercise, mainly as a result of increasing perfusion of areas of high VA/Q [A-a]D0₂(0 was greater than predicted, becoming significant during heavy exercise, indicating diffusion limitation. Cardiac output increased from 6.9±0.9 1-min-1 (R) to 25.2±2.5 1-min-1 at 300W and 33.3±3.7 1-min-1 at maximal exercise. End diastolic volume increased from R to heavy exercise (p < 0.001), accompanied by a decrease in end systolic volume (p =0.05). Stroke volume and ejection fraction also increased significantly from R to 300W (p <0.001). Deconvolution PTT decreased from 9.32±1.41 s at rest to 2.91±0.30 s during max exercise and was highly correlated with centroid PTT both at rest (r=0.99, p<0.001) and during maximal exercise (r=0.96, p<0.001). PTT during maximal exercise was significantly correlated with Pa0₂ (1=0.65, p<0.05) and [A-a]D0₂(0)_[A-a]D0₂(p) (r=-0.60, p<0.05). Calculated pulmonary blood volume increased during maximal exercise by 57% over resting values to over 25% of total blood volume and when corrected for body surface area correlated significantly with Pa0₂ (r=0.69, p<0.05). There was a significant correlation between (A-a)D, PTT, the ventilatory equivalent for CO₂ and Pa0₂ during maximal exercise (r=0.94, p<0.01) allowing prediction of over 80% of the variance in Pa0₂ between subjects. These data indicate that highly trained athletes develop VA/Q mismatch accompanied by diffusion limitation during maximal exercise. Observed decrease in Pa0₂2 during high intensity exercise is the result of a complex interaction between VA/Q mismatch, hypoventilation and diffusion limitation secondary to shortened pulmonary transit.

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Books on the topic "Respiration Blood gases"

1

Shapiro, Barry A. Clinical application of blood gases. 5th ed. Chicago, IL: Mosby-Year Book, 1993.

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Shapiro, Barry A. Clinical application of blood gases. 5th ed. St. Louis: Mosby, 1994.

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3

F, Walker Jerome, ed. Clinical arterial blood gas analysis. St. Louis: Mosby, 1987.

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4

Ventilation/blood flow and gas exchange. 4th ed. Oxford [Oxfordshire]: Blackwell Scientific Publications, 1985.

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5

The effects of pursed-lip breathing and added expiratory resistences on arterialized-venous blood gases and lactic acid. 1988.

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The effects of pursed-lip breathing and added expiratory resistences on arterialized-venous blood gases and lactic acid. 1988.

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The effects of pursed-lip breathing and added expiratory resistences on arterialized-venous blood gases and lactic acid. 1988.

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The effects of pursed-lip breathing and added expiratory resistences on arterialized-venous blood gases and lactic acid. 1988.

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9

Garby, Lars. The Respiratory Functions of Blood. Springer, 2012.

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The effects of pursed-lip breathing and added expiratory resistances on arterialized-venous blood gases and lactic acid. 1986.

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Book chapters on the topic "Respiration Blood gases"

1

Amin-Naves, Jalile, A. P. Sanchez, M. Bassi, H. Giusti, F. T. Rantin, and M. L. Glass. "Blood Gases of the South American Lungfish, Lepidosiren paradoxa: A Comparison to Other Air-breathing Fish and to Amphibians." In Fish Respiration and Environment, 243–54. CRC Press, 2016. http://dx.doi.org/10.1201/b11000-13.

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Craig, Anne, and Anthea Hatfield. "Monitoring and equipment." In The Complete Recovery Room Book, 59–76. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198846840.003.0004.

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Routine monitoring is an essential part of recovery room procedure. Respiration, a vital concern while awakening after anaesthesia, is given specific attention with reference to modern capnography. This chapter also describes additional monitoring in detail: pulse oximetry, blood pressure, central venous pressure, and arterial blood gases are clearly described. A comprehensive description of electrocardiography guides the student through this complicated subject. The monitoring of temperature and warming blankets, with suggestions for purchasing equipment, are included.

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