CO2transport in normovolemic anemia: complete compensation and stability of blood CO2tensions

1997 ◽  
Vol 83 (1) ◽  
pp. 240-246 ◽  
Author(s):  
Steven Deem ◽  
Michael K. Alberts ◽  
Michael J. Bishop ◽  
Akhil Bidani ◽  
Erik R. Swenson
Keyword(s):  
Minute Ventilation ◽  
Venous Blood ◽  
Calculated Data ◽  
Blood Gases ◽  
Physiological Basis ◽  
Mechanically Ventilated ◽  
Physiological Dead Space ◽  
Normovolemic Anemia ◽  
The Mathematical Model

Deem, Steven A., Michael K. Alberts, Michael J. Bishop, Akhil Bidani, and Erik R. Swenson.CO2transport in normovolemic anemia: complete compensation and stability of blood CO2tensions. J. Appl. Physiol. 83(1): 240–246, 1997.—Isovolemic hemodilution does not appear to impair CO2elimination nor cause CO2retention despite the important role of red blood cells in blood CO2transport. We studied this phenomenon and its physiological basis in eight New Zealand White rabbits that were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Isovolemic anemia was induced by simultaneous blood withdrawal and infusion of 6% hetastarch in sequential stages; exchange transfusions ranged from 15–30 ml in volume. Variables measured after each hemodilution included hematocrit (Hct), arterial and venous blood gases, mixed expired[Formula: see text] and[Formula: see text], and blood pressure; also, O2consumption, CO2production, cardiac output (Q˙), and physiological dead space were calculated. Data were analyzed by comparison of changes in variables with changes in Hct and by using the model of capillary gas exchange described by Bidani ( J. Appl. Physiol. 70: 1686–1699, 1991). There was complete compensation for anemia with stability of venous and arterial [Formula: see text]between Hct values of 36 ± 3 and 12 ± 1%, which was predicted by the mathematical model. Over this range of hemodilution,Q˙ rose 50%, and the O2extraction ratio increased 61% without a decline in CO2production or a rise in alveolar ventilation. The dominant compensations maintaining CO2transport in normovolemic anemia include an increasedQ˙ and an augmented Haldane effect arising from the accompanying greater O2extraction.

Ventilatory and metabolic adaptations to walking and cycling in patients with COPD

2000 ◽  
Vol 88 (5) ◽  
pp. 1715-1720 ◽  
Author(s):  
Paolo Palange ◽  
Silvia Forte ◽  
Paolo Onorati ◽  
Felice Manfredi ◽  
Pietro Serra ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Venous Blood ◽  
Blood Gases ◽  
Peak Exercise ◽  
Chronic Obstructive ◽  
Arterial Blood Gases ◽  
Physiological Dead Space ◽  
Arterial Blood ◽  
Ergometer Exercise ◽  
Walking Capacity

To test the hypothesis that in chronic obstructive pulmonary disease (COPD) patients the ventilatory and metabolic requirements during cycling and walking exercise are different, paralleling the level of breathlessness, we studied nine patients with moderate to severe, stable COPD. Each subject underwent two exercise protocols: a 1-min incremental cycle ergometer exercise (C) and a “shuttle” walking test (W). Oxygen uptake (V˙o 2), CO2output (V˙co 2), minute ventilation (V˙e), and heart rate (HR) were measured with a portable telemetric system. Venous blood lactates were monitored. Measurements of arterial blood gases and pH were obtained in seven patients. Physiological dead space-tidal volume ratio (Vd/Vt) was computed. At peak exercise, W vs. CV˙o 2,V˙e, and HR values were similar, whereasV˙co 2 (848 ± 69 vs. 1,225 ± 45 ml/min; P < 0.001) and lactate (1.5 ± 0.2 vs. 4.1 ± 0.2 meq/l; P < 0.001) were lower, ΔV˙e/ΔV˙co 2(35.7 ± 1.7 vs. 25.9 ± 1.3; P < 0.001) and ΔHR/ΔV˙o 2values (51 ± 3 vs. 40 ± 4; P < 0.05) were significantly higher. Analyses of arterial blood gases at peak exercise revealed higher Vd/Vt and lower arterial partial pressure of oxygen values for W compared with C. In COPD, reduced walking capacity is associated with an excessively high ventilatory demand. Decreased pulmonary gas exchange efficiency and arterial hypoxemia are likely to be responsible for the observed findings.

scholarly journals Postpneumonectomy alveolar growth does not normalize hemodynamic and mechanical function

1999 ◽  
Vol 87 (2) ◽  
pp. 491-497 ◽  
Author(s):  
Shin-Ichi Takeda ◽  
Murugappan Ramanathan ◽  
Aaron S. Estrera ◽  
Connie C. W. Hsia
Keyword(s):  
Cardiac Output ◽  
Minute Ventilation ◽  
Lung Resection ◽  
Venous Blood ◽  
Structural Response ◽  
Respiratory Muscles ◽  
Blood Gases ◽  
Mixed Venous Blood ◽  
Power Requirement ◽  
Normal Mean

Immature foxhounds underwent 55% lung resection by right pneumonectomy ( n = 5) or thoracotomy without pneumonectomy (Sham, n = 6) at 2 mo of age. Cardiopulmonary function was measured during treadmill exercise on reaching maturity 1 yr later. In pneumonectomized animals compared with Sham animals, maximal oxygen uptake, ventilatory response, and cardiac output during exercise were normal. Arterial and mixed venous blood gases and arteriovenous oxygen extraction during exercise were also normal. Mean pulmonary arterial pressure and resistance were elevated at a given cardiac output. Dynamic ventilatory power requirement was also significantly elevated at a given minute ventilation. These long-term hemodynamic and mechanical abnormalities are in direct contrast to the normal pulmonary gas exchange during exercise in these same pneumonectomized animals reported elsewhere (S. Takeda, C. C. W. Hsia, E. Wagner, M. Ramanathan, A. S. Estrera, and E. R. Weibel. J. Appl. Physiol. 86: 1301–1310, 1999). Functional compensation was superior in animals pneumonectomized as puppies than as adults. These data indicate a limited structural response of conducting airways and extra-alveolar pulmonary blood vessels to pneumonectomy and suggest the development of other sources of adaptation such as those involving the heart and respiratory muscles.

A respiratory venous chemoreceptor in the young puppy

1975 ◽  
Vol 38 (5) ◽  
pp. 819-826 ◽  
Author(s):  
K. R. Kollmeyer ◽  
L. I. Kleinman
Keyword(s):  
Minute Ventilation ◽  
Venous Blood ◽  
Blood Gases ◽  
High Ratio ◽  
Mixed Venous Blood ◽  
Extracorporeal Circuit ◽  
Shunt System ◽  
Newborn Animal ◽  
Venous Circulation ◽  
Arterial Blood

An extracorporeal venovenous shunt system utilizing a membrane oxygenator to alter venous blood gases was used to study the regulation of ventilation in 28 newborn and 4 adult dogs. There was no effect of the extracorporeal circuit per se (without the oxygenator in the system) on essential cardiovascular or respiratory function. When the puppies were placed on the extracorporeal circuit with the oxygenator in the system to effect changes in mixed venous blood gas composition there was a significant increase in venous P02 (Pv02), a decrease in venous Pco2 (Pvco2), a rise in venous pH (PHv), and a marked fall in minute ventilation (VE). There were no significant changes in cardiovascular function or arterial blood gases to account for the depression of ventilation. Acute changes in Pvo2 produced appropriate directional changes of VE under conditions where other arterial and venous blood gases were held constant. At a low Pvco2/Paco2 ratio, ventilation was depressed compared to those conditions with a high ratio. At any Pvc02/Paco2 ratio, ventilation could be depressed by raising the Pvo2. In adult animals ventilation could not be altered by changing venous blood gases. These experiments support the existence of a respiratory chemoreceptor sensitive to both PO2 and PCO2 in the prepulmonary or venous circulation of the newborn animal.

Topic role of venous blood gases in patients of acute breathlessness presenting in emergency department

2019 ◽  
Vol 11 (1) ◽  
pp. 94-98
Author(s):  
Deepali Rajpal ◽  
◽  
Utkarsh Khandelwal ◽  
Manhar Shah ◽  
Manu Mathew Lal ◽  
...  
Keyword(s):  
Emergency Department ◽  
Venous Blood ◽  
Blood Gases

scholarly journals Importance of the lactate anion in control of breathing

1998 ◽  
Vol 84 (2) ◽  
pp. 411-416 ◽  
Author(s):  
Thorir Hardarson ◽  
Jon O. Skarphedinsson ◽  
Torarinn Sveinsson
Keyword(s):  
Wistar Rats ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Sodium Lactate ◽  
Control Of Breathing ◽  
Strenuous Exercise ◽  
Blood Samples ◽  
Arterial Concentration ◽  
Spontaneously Breathing

Hardarson, Thorir, Jon O. Skarphedinsson, and Torarinn Sveinsson. Importance of the lactate anion in control of breathing. J. Appl. Physiol. 84(2): 411–416, 1998.—The purpose of this study was to examine the effects of raising the arterial La− and K+ levels on minute ventilation (V˙e) in rats. Either La− or KCl solutions were infused in anesthetized spontaneously breathing Wistar rats to raise the respective ion arterial concentration ([La−] and [K+]) gradually to levels similar to those observed during strenuous exercise.V˙e, blood pressure, and heart rate were recorded continuously, and arterial [La−], [K+], pH, and blood gases were repeatedly measured from blood samples. To prevent changes in pH during the La−infusions, a solution of sodium lactate and lactic acid was used. Raising [La−] to 13.2 ± 0.6 (SE) mM induced a 47.0 ± 4.0% increase inV˙e without any concomitant changes in either pH or [Formula: see text]. Raising [K+] to 7.8 ± 0.11 mM resulted in a 20.3 ± 5.28% increase inV˙e without changes in pH. Thus our results show that La−itself, apart from lactic acidosis, may be important in increasingV˙e during strenuous exercise, and we confirm earlier results regarding the role of arterial [K+] in the control ofV˙e during exercise.

Brain ECF pH and central chemical control of ventilation during anoxia in turtles

1987 ◽  
Vol 252 (5) ◽  
pp. R848-R852 ◽  
Author(s):  
D. G. Davies ◽  
J. A. Sexton
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Control Period ◽  
Extracellular Fluid ◽  
Blood Gases ◽  
Breathing Frequency ◽  
Arterial Blood Gases ◽  
Brain Extracellular Fluid ◽  
Arterial Blood

The role of changes in brain extracellular fluid [H+] in the control of breathing during anoxia was studied in unanesthetized turtles, Chrysemys scripta. Ventilation, [minute ventilation (VE), tidal volume (VT), and breathing frequency (f)], cerebral extracellular fluid (ECF) pH, and arterial blood gases were measured at 25 degrees C during a 30-min control period (room air), 30 min of anoxia (100% N2 breathing), and 60 min of recovery (room air). ECF pH was measured in the cerebral cortex with a glass microelectrode (1-2 micron tip diam). Large changes in ventilation, ECF [H+], and arterial blood gases were observed. The predominant ventilatory response was an increase in f with a slight increase in VT. A correlation was observed between ECF [H+] and f, which suggested that central chemoreceptor stimulation was involved in the ventilatory response.

Effect of brain blood flow on hypoxic ventilatory response in humans

1987 ◽  
Vol 63 (3) ◽  
pp. 1100-1106 ◽  
Author(s):  
M. Nishimura ◽  
A. Suzuki ◽  
Y. Nishiura ◽  
H. Yamamoto ◽  
K. Miyamoto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Venous Blood ◽  
Blood Gases ◽  
Interindividual Variation ◽  
Brain Blood Flow ◽  
Hypoxic Ventilatory Response ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

To assess the effect of brain blood flow on hypoxic ventilatory response, we measured arterial and internal jugular venous blood gases and ventilation simultaneously and repeatedly in eight healthy male humans in two settings: 1) progressive and subsequent sustained hypoxia, and 2) stepwise and progressive hypercapnia. Ventilatory response to progressive isocapnic hypoxia [arterial O2 partial pressure 155.9 +/- 4.0 (SE) to 46.7 +/- 1.5 Torr] was expressed as change in minute ventilation per change in arterial O2 saturation and varied from -0.16 to -1.88 [0.67 +/- 0.19 (SE)] l/min per % among subjects. In the meanwhile, jugular venous PCO2 (PjCO2) decreased significantly from 51.0 +/- 1.1 to 47.3 +/- 1.0 Torr (P less than 0.01), probably due to the increase in brain blood flow, and stayed at the same level during 15 min of sustained hypoxia. Based on the assumption that PjCO2 reflects the brain tissue PCO2, we evaluated the depressant effect of fall in PjCO2 on hypoxic ventilatory response, using a slope for ventilation-PjCO2 line which was determined in the second set of experiments. Hypoxic ventilatory response corrected with this factor was -1.31 +/- 0.33 l/min per %, indicating that this factor modulated hypoxic ventilatory response in humans. The ventilatory response to progressive isocapnic hypoxia did not correlate with this factor but significantly correlated with the withdrawal test (modified transient O2 test), which was performed on a separate day. Accordingly we conclude that an increase in brain blood flow during exposure to moderate hypoxia may substantially attenuate the ventilatory response but that it is unlikely to be the major factor of the interindividual variation of progressive isocapnic hypoxic ventilatory response in humans.

Alveolar slope and dead space of He and SF6 in dogs: comparison of airway and venous loading

1990 ◽  
Vol 69 (3) ◽  
pp. 937-944 ◽  
Author(s):  
M. Meyer ◽  
K. D. Schuster ◽  
H. Schulz ◽  
M. Mohr ◽  
J. Piiper
Keyword(s):  
Partial Pressure ◽  
Dead Space ◽  
Venous Blood ◽  
Inert Gases ◽  
Volume Distribution ◽  
Mechanically Ventilated ◽  
Alveolar Plateau ◽  
Single Breath ◽  
Sequential Emptying

Series (Fowler) dead space (VD) and slope of the alveolar plateau of two inert gases (He and SF6) with similar blood-gas partition coefficients (approximately 0.01) but different diffusivities were analyzed in 10 anesthetized paralyzed mechanically ventilated dogs (mean body wt 20 kg). Single-breath constant-flow expirograms were simultaneously recorded in two conditions: 1) after equilibration of lung gas with the inert gases at tracer concentrations [airway loading (AL)] and 2) during steady-state elimination of the inert gases continuously introduced into venous blood by a membrane oxygenator and partial arteriovenous bypass [venous loading (VL)]. VD was consistently larger for SF6 than for He, but there was no difference between AL and VL. The relative alveolar slope, defined as increment of partial pressure per increment of expired volume and normalized to mixed expired-inspired partial pressure difference, was larger by a factor of two in VL than in AL for both He and SF6. The He-to-SF6 ratio of relative alveolar slope was generally smaller than unity in both VL and AL. Whereas unequal ventilation-volume distribution combined with sequential emptying of parallel lung regions appears to be responsible for the sloping alveolar plateau during AL, the steeper slope during VL is attributed to the combined effects of continuing gas exchange and ventilation-perfusion inequality coupled with sequential emptying. The differences between He and SF6 point at the contributing role of diffusion-dependent mechanisms in intrapulmonary gas mixing.

Diaphragm metabolism during supramaximal phrenic nerve stimulation

1989 ◽  
Vol 66 (2) ◽  
pp. 567-572 ◽  
Author(s):  
A. Pope ◽  
S. M. Scharf ◽  
R. Brown
Keyword(s):  
Phrenic Nerve ◽  
Venous Blood ◽  
Lactate Production ◽  
Rest Period ◽  
Blood Gases ◽  
Base Line ◽  
Transdiaphragmatic Pressure ◽  
Mechanically Ventilated ◽  
Significant Difference ◽  
Lactate Levels

The metabolic changes accompanying diaphragm fatigue caused by supramaximal stimulation of the phrenic nerves are incompletely described. In particular, we wished to determine whether the occurrence of anaerobic metabolism correlated with fatigue as defined by decline in force generation. In 10 anesthetized mechanically ventilated mongrel dogs we measured arterial pressure, transdiaphragmatic pressure (Pdi), phrenic arterial flow (Qdi-Doppler flow probe), arterial and phrenic venous blood gases, and lactate levels. From these we derived indexes of diaphragm O2 consumption (VO2) and lactate production. Bilateral phrenic nerve pacing was carried out (50 Hz, duty cycle 0.4, 24 contractions/min) for two 15-min pacing periods separated by a 45-min rest period. Over each pacing period Pdi decreased from approximately 16 to approximately 10 cmH2O (P less than 0.01, no significant difference between periods). Initially, during pacing, Qdi and VO2 each increased fivefold over prepacing base line. Qdi remained elevated at this level whereas VO2 decreased over the pacing period by approximately 25%. Hence, the change in VO2 over the pacing period was due primarily to changes in O2 extraction. During the first pacing period lactate production was observed early and declined throughout the pacing period. No lactate production was observed during the second pacing period, although Pdi, VO2, and Qdi responses were the same for both pacing periods. Phrenic venous PO2 remained greater than 30 Torr throughout both pacing periods.(ABSTRACT TRUNCATED AT 250 WORDS)

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